DE112022000047T5 - MEDICAL COMPOSITION FOR THE TREATMENT OR REDUCTION OF HANGOVERS DUE TO ALCOHOL AND USE THEREOF - Google Patents

Abstract

A medicinal composition for treating or reducing alcohol hangover is provided comprising Radix Codonopsis, Pericarpium Citri Reticulatae, and Poria cocos (Schw.) Wolf, and Rhizoma Zingiberis and Rhizoma Atractylodis Macrocephalae. Further provided is the use of an effective amount of the medicinal composition in the manufacture of a medicine for the treatment or reduction of hangover and damage to the liver, kidney and intestinal tract.

Description

technical field

The invention relates to a new medicinal composition for the treatment or reduction of hangover and damage to the liver, kidney and intestinal tract.

State of the art

Alcohol-induced hangover is the most commonly reported adverse effect of excessive alcohol consumption and occurs when blood alcohol concentration (BAC) returns to approximately zero. Because ethanol is miscible with water, the water-rich tissues, such as the brain, are targeted, resulting in well-known syndromes such as pain, headache, fatigue, attention deficit disorder, thirst, dizziness, nausea, cognitive impairment, and emotional alternation. The hangover leads to illicit absences from work, impaired job performance, reductions in productivity, poor academic performance, and even threats to engage in potentially hazardous activities of daily living, such as driving a vehicle or operating heavy machinery. Compared to other common diseases and other health-threatening factors, the hangover brings with it a much more serious social and scientific problem, as well as a much higher health threat.

The search for a method to alleviate alcohol-induced damage and its side effects (including hangovers) began long ago, from the time alcohol was first produced. Although many methods of treatment and prevention are available, scientific evidence of their effectiveness is generally lacking.

Therefore, there is a need for methods and compositions that rapidly reduce the syndromes associated with elevation of blood alcohol concentration (BAC), promote rapid recovery from alcohol consumption, or reduce alcohol consumption-related syndromes or the syndromes prevent. The invention addresses these and other needs.

Disclosure of Invention

In one embodiment, the invention discloses a medicinal composition comprising: (1) an herbal blend comprising at least two herbs selected from the group consisting of: Rhizoma Zingiberis; radix codonopsis; Poria cocos (Schw.) wolf; Pericarpium Citri Reticulatae and Rhizoma Atractylodis Macrocephalae; and (2) a pharmaceutically acceptable carrier.

In a further embodiment there is provided a medicinal composition comprising: (1) an herbal mixture containing Radix Codonopsis, Poria cocos (Schw.) Wolf, and Pericarpium Citri Reticulatae; and (2) a pharmaceutically acceptable carrier.

In a further embodiment there is provided a medicinal composition comprising: (1) a herbal mixture containing Rhizoma Zingiberis, Radix Codonopsis, Poria cocos (Schw.) Wolf, Pericarpium Citri Reticulatae and Rhizoma Atractylodis Macrocephalae; and (2) a pharmaceutically acceptable carrier.

The invention further relates to the use of the medicinal composition described herein in the manufacture of a medicine for treating or reducing the influence of alcohol consumption.

The invention further relates to the use of the medicinal composition described herein in the manufacture of a medicine for treating or reducing inflammation of liver cells and fat accumulation.

The invention further relates to the use of the medicinal composition described herein in the manufacture of a medicine for the treatment or reduction of damage to the function of the mucous membrane of the small intestine or the intestine.

The invention further relates to the use of the medicinal composition described herein in the manufacture of a medicine for the treatment or reduction of damage to the glomerulus or function of the kidney.

The invention further relates to a method of treating or reducing alcohol consumption interference for individuals in need by administering the medicinal composition described herein.

As used herein, the terms "the invention" or "the present invention" are intended to mean all subject matter within the scope of this patent and the claims that follow. The statement containing these terms should not be taken as limiting either the subject matter described herein or the meaning or scope of the claims. The embodiments covered by the present patent are not defined by the content in the "Disclosure of the Invention" part but by the following claims. The "Disclosure of the Invention" part describes the various aspects of the invention in a very conceptual manner and briefly introduces the terms that are further described below in the "Detailed Embodiments" part. The "Disclosure of the Invention" part does not relate to identifying the essential or fundamental features of the claimed subject matter or solely to defining the scope of the claimed subject matter. The subject matter should be understood in the context of the appropriate parts of the entire specification, any or all figures, and the scope of each of the claims.

The invention will be clearer considering the following figures and the embodiments.

character list

• 1 Fig. 12 is a line graph for explaining the effect of the medicinal composition of the present invention on the body weight of mice.
• 2 and 3 are histograms to explain the influence of the medicinal composition according to the invention on the liver weight/body weight or kidney weight/body weight ratio of mice.
• 4 and 5 are histograms for explaining the influence of the medicinal composition according to the invention on the serum liver function (AST and ALT) of mice.
• 6 and 7 are histograms for explaining the effect of the medicinal composition of the present invention on the total cholesterol level (T-CHO) and triglyceride level (TG) in the serum of mice.
• 8th Fig. 12 is a histogram for explaining the effect of the medicinal composition of the present invention on the serum glucose level of mice.
• 9 and 10 are histograms for explaining the influence of the medicinal composition of the present invention on the total cholesterol (T-CHO) level and triglyceride (TG) level in the liver of mice.
• 11 Fig. 12 is a histogram for explaining scores for treatment of steatosis in mice with alcoholic liver disease by the medicinal composition of the present invention.
• 12 Fig. 12 is a histogram for explaining the effect of an embodiment of the medicinal composition of the present invention on the performance in the field fasting test.
• 13 Fig. 12 is a histogram for explaining the effect of the medicinal composition of the present invention on alcohol-induced syndromes at 1 hour after alcohol consumption.
• 14 Fig. 12 is a histogram for explaining the effect of the medicinal composition of the present invention on alcohol-induced syndromes at 2 hours after alcohol consumption.
• 15 Fig. 12 is a histogram for explaining the effect of the medicinal composition of the present invention on alcohol-induced syndromes at 24 hours after alcohol consumption.
• 16A until 16C are histograms for explaining the influence of an embodiment of the medicinal composition according to the invention on the liver function tests (AST, ALT and γ-GT).
• 17A and 17B are histograms for explaining the influence of an embodiment of the medicinal composition according to the invention on the kidney function tests (aldosterone and creatinine).
• 18 Fig. 12 is a histogram for explaining the effect of an embodiment of the medicinal composition of the present invention on glucose-6-phosphate dehydrogenase (G6PD).
• 19 Figure 13 is a set of photographs under hematoxylin-eosin (H&E) staining showing alcohol-induced jejunal villous damage (Figure B) and alcohol-induced small intestinal barrier damage reduced by the medicinal composition of the present invention ( to E) are shown.
• 20 Figure 12 is a set of H&E images showing alcohol-induced glomerular damage (panel B) and alcohol-induced glomerular damage reduced by the medicinal composition of the present invention ( to E) are shown.

Detailed Embodiments

definitions

As used previously and throughout the text of the disclosure, the following terms have the respective meanings unless otherwise specified.

As used herein, the singular form "a" and "the" of a term includes the plural form as well, unless otherwise specified.

As used herein, "effective amount" means such an amount that a medicinal composition can achieve the treatment or amelioration of at least one syndrome induced by alcohol consumption or BAC elevation.

As used herein, the term "treatment" means palliative use and/or slowing or suppressing the progression of an alcohol-induced syndrome or symptom.

As used herein, the term "individual" means a human or other animal with or suspected of having an alcohol consumption or BAC elevation-induced syndrome. Thus, an alcohol consuming individual is included within the scope of the term 'individual' regardless of whether they exhibit a syndrome or symptom due to alcohol use or BAC elevation.

All numbers herein can be considered modified with "about". As used herein, the term "about" covers a deviation of ±10%.

In one embodiment, the invention discloses a medicinal composition comprising: (1) an herbal blend comprising at least two herbs selected from the group consisting of: Rhizoma Zingiberis; radix codonopsis; Poria cocos (Schw.) wolf; Pericarpium Citri Reticulatae and Rhizoma Atractylodis Macrocephalae; and (2) a pharmaceutically acceptable carrier.

In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis and Radix Codonopsis. In an exemplary embodiment, the herbal blend contains radix codonopsis and poria cocos (black) wolf. In an exemplary embodiment, the herbal blend includes Poria cocos (Schw.) Wolf and Pericarpium Citri Reticulatae. In an exemplary embodiment, the herbal blend includes Pericarpium Citri Reticulatae and Rhizoma Atractylodis Macrocephalae. In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis and Poria cocos (Schw.) Wolf. In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis and Pericarpium Citri Reticulatae. In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis and Rhizoma Atractylodis Macrocephalae. In an exemplary embodiment, the herbal blend includes radix codonopsis and pericarpium citri reticulatae. In an exemplary embodiment, the herbal blend includes Radix Codonopsis and Rhizoma Atractylodis Macrocephalae. In an exemplary embodiment, the herbal blend includes Poria cocos (Schw.) Wolf and Rhizoma Atractylodis Macrocephalae.

In a further embodiment, the invention discloses a medicinal composition comprising: (1) a herbal mixture comprising at least three herbs selected from the group of best derived from: Rhizoma Zingiberis; radix codonopsis; Poria cocos (Schw.) Wolf, Pericarpium Citri Reticulatae and Rhizoma Atractylodis Macrocephalae; and (2) a pharmaceutically acceptable carrier.

In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis, Radix Codonopsis, and Poria cocos (Schw.) Wolf. In an exemplary embodiment, the herbal blend includes Radix Codonopsis, Poria cocos (Schw.) Wolf, and Pericarpium Citri Reticulatae. In an exemplary embodiment, the herbal blend includes Poria cocos (Schw.) Wolf, Pericarpium Citri Reticulatae, and Rhizoma Atractylodis Macrocephalae. In an exemplary embodiment, the herbal blend includes Pericarpium Citri Reticulatae, Rhizoma Atractylodis Macrocephalae, and Rhizoma Zingiberis. In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis, Pericarpium Citri Reticulatae, and Rhizoma Atractylodis Macrocephalae. In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis, Radix Codonopsis, and Pericarpium Citri Reticulatae. In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis, Poria cocos (Schw.) Wolf, and Rhizoma Atractylodis Macrocephalae. In an exemplary embodiment, the weight ratio of Radix Codonopsis: Pericarpium Citri Reticulatae: Poria cocos (Schw.) Wolf in the herbal mixture is about 25-35%: 25-35%: 30-50%.

In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis, Radix Codonopsis, and Rhizoma Atractylodis Macrocephalae. In an exemplary embodiment, the herbal blend includes Rhizoma Zingiberis, Poria cocos (Schw.) Wolf, and Rhizoma Atractylodis Macrocephalae.

In an exemplary embodiment, the herbal blend includes Radix Codonopsis, Pericarpium Citri Reticulatae, and Rhizoma Atractylodis Macrocephalae. In an exemplary embodiment, the herbal blend includes Radix Codonopsis, Poria cocos (Schw.) Wolf, and Rhizoma Atractylodis Macrocephalae.

In a further embodiment, the invention discloses a medicinal composition comprising: (1) an herbal mixture containing Rhizoma Zingiberis, Radix Codonopsis, Poria cocos (Schw.) Wolf, Pericarpium Citri Reticulatae and Rhizoma Atractylodis Macrocephalae; and (2) a pharmaceutically acceptable carrier.

In an exemplary embodiment, the herbal mixture contains about 5-15% by weight of Rhizoma zingiberis. In an exemplary embodiment, the herbal blend contains about 15-25% by weight radix codonopsis. In an exemplary embodiment, the herbal mixture contains about 25-35% by weight Poria cocos (Schw.) Wolf. In an exemplary embodiment, the herbal blend contains about 15-25% by weight Pericarpium Citri Reticulatae. In an exemplary embodiment, the herbal mixture contains about 10-20% by weight of Rhizoma Atractylodis Macrocephalae. In an exemplary embodiment, the herbal mixture contains about 20-25% by weight Radix Codonopsis, about 30-35% by weight Poria cocos (Schw.) Wolf, about 20-25% by weight Pericarpium Citri Reticulatae, about 15-18 % by weight Rhizoma Atractylodis Macrocephalae, and about 6-12% by weight Rhizoma Zingiberis.

In an exemplary embodiment, the herbal mixture is a dried powder or freeze-dried powder of at least two of the herbs listed (i.e. Rhizoma Zingiberis, Radix Codonopsis, Poria cocos (Schw.) Wolf, Pericarpium Citri Reticulatae and Rhizoma Atractylodis Macrocephalae). In an exemplary embodiment, the herbal mixture is an aqueous or alcoholic extract of at least two of the herbs listed (i.e. Rhizoma Zingiberis, Radix Codonopsis, Poria cocos (Schw.) Wolf, Pericarpium Citri Reticulatae and Rhizoma Atractylodis Macrocephalae).

The herbs in the herbal blend can be in their original forms, dried powder, freeze-dried powder, ground powder, decoction, aqueous or alcoholic extract, or extracted particles. In an exemplary embodiment, the herbal mixture is prepared by aqueous extraction, whereby the original herbs (optionally ground before extraction to obtain an optimal extraction result) are heated in water or in a solvent and then filtered and concentrated (the liquid extract is Concentration thickened at vacuum or subatmospheric pressure).

• kleine Schäden (BAC zwischen 0,0 - 0,05%): leichte Schäden bezüglich Sprachvermögen, Gedächtnis, Aufmerksamkeit, Koordination und Bilanz, Relaxation, und Schläfrigkeit;
• moderate Schäden (BAC-Niveau zwischen 0,06 - 0,15%): erhöhtes Angriffsrisiko, weitere Schäden bezüglich Sprachvermögen, Gedächtnis, Aufmerksamkeit, Koordination, Bilanz und Fahrfähigkeiten;
• schwere Schäden (BAC-Niveau zwischen 0,16 - 0,30%): erhebliche Schäden bezüglich Sprachvermögen, Gedächtnis, Aufmerksamkeit, Koordination, Bilanz, Bestimmung und Entscheidung, Verwirrtheit, Ohnmacht, Schwindel und Übelkeit, Bewusstlosigkeit, Emotionswechsel und unregelmäßiges Atmen;
• lebensbedrohliche Schäden (übermäßiger Alkoholkonsum, BAC 0,31 - 0,45%):
  • Verwirrtheit, Bewusstlosigkeit, epileptischer Anfall und Hypothermie.

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) breaks down the damage associated with increasing blood alcohol concentration (BAC) into the following levels:

• minor damage (BAC between 0.0 - 0.05%): slight damage to speech, memory, attention, coordination and balance, relaxation, and sleepiness;
• moderate damage (BAC level between 0.06 - 0.15%): increased risk of attack, further damage to speech, memory, attention, coordination, balance and driving skills;
• severe damage (BAC level between 0.16 - 0.30%): significant damage in terms of language ability, memory, attention, coordination, balance, determination and decision-making, confusion, fainting, dizziness and nausea, unconsciousness, change of emotions and irregular breathing;
• life-threatening damage (excessive alcohol consumption, BAC 0.31 - 0.45%):
  • Confusion, unconsciousness, epileptic seizure and hypothermia.

A hangover is a group of syndromes resulting from excessive alcohol consumption. The typical syndromes include fatigue, exhaustion, thirst, headache, sore muscles, nausea, abdominal pain, dizziness, sensitivity to light and noise, anxiety, irritability, sweating and an increase in blood pressure.

For example, it is desirable to take the medicinal composition before, during, or shortly after consuming any amount of alcohol in a social activity so that the syndromes and symptoms associated with BAC elevation are reduced and the drinker sobers up quickly. In addition, it is desirable to use the medicinal composition for the treatment and prevention of damage to the gastrointestinal tract and urinary tract such as damage to the liver, kidney or intestinal tract.

The invention relates to a method of reducing or treating the effects of alcohol consumption on individuals in need by administering the medicinal composition described herein.

The non-limiting examples of influencing alcohol consumption include syndromes and symptoms with blood alcohol concentration increase or hangover.

The medicinal composition can be formulated or prepared with an easily usable and pharmaceutically acceptable carrier for the herbal mixture. The pharmaceutically acceptable carrier can contain physiologically acceptable compounds, for example to stabilize or increase or decrease the absorption or clearance of the medicinal composition according to the invention. Physiologically acceptable compounds include, for example, carbohydrates such as glucose, sucrose, or polydextrose; antioxidants such as ascorbic acid or glutathione; chelator; low molecular weight proteins; catcher; carriers for lipids; or other stabilizers and/or buffering agents. Such a preparation can be made by various technologies, including combining an herbal mixture with a suitable, pharmaceutically acceptable carrier (such as a liquid carrier, solid carrier, or both).

The medicinal composition provided herein optionally comprises antioxidants, buffering agents, antibacterial agents, suspending agents, thickeners, preservatives, co-solvents, tackifiers or other therapeutic components for the treatment of alcohol syndrome, such as acamprosate, gabapentin (trade name NEURONTIN), or topiramate (trade name Topamax) . In terms of compatibility with the medicinal composition and safety for the individual, the carrier and other treatment components must be acceptable.

The medicinal composition is administered in an amount effective to reduce the individual's syndromes or symptoms due to BAC elevation. The dose of the medicinal composition administered depends on the amount of alcohol consumed and other clinical factors such as body weight and general conditions of the individual, as well as the route of administration. The useful dose of the medicinal composition provided herein is determined by comparing their in vitro and in vivo activities in experimental animals. It is already known in this art how to extrapolate the effective dose for mice or other animals into a dose for a human. On the American Patent No. 4,938,949 may be referenced, which is hereby incorporated by reference.

According to the method provided herein, the medicinal composition can be delivered in any of the following ways, including but not limited to such. B. subcutaneous, intramuscular, intravenous, intraarterial, intraperitoneal, intracutaneous, intravitreal; on the skin; transdermal; percutaneously; orally, such as B. in the form of lozenge, powder, pill, lozenge, capsule, liquid, edible foil or in any other form suitable for herbs; implantable osmotic pump; suppositories; aerosol spray; local; on the eyes; nasal inhalation; pulmonary inhalation or imprinting in the skin. In one embodiment, the medicinal composition of the present invention can be administered orally as an aqueous extract.

The medicinal composition can be administered once or repeatedly over a period of time. The medicinal composition can conveniently be used at a suitable time interval, such as e.g. B. once a day, twice a day, three times a day, four times a day, six times a day, once every two days, once every three days, etc.

The method described herein also encompasses a method of investigation and its use, including in vitro and in vivo methods for treating or reducing the effect on an individual of consumption of any amount of alcohol.

The embodiments of the invention are described by the following working examples, which should in no way be construed as limiting the scope of the invention. Unless otherwise noted, the investigations in working examples below follow the well-known flow. Some processes are described below for explanation.

example

Example 1: Case Study of Effect of Medicinal Composition on Mice

This study aims to protect against alcoholic liver damage in experimental mice with alcoholic liver disease by medicinal compositions S1-S11, and the components of medicinal compositions S1-S11 are shown in Table 1 ("√" represents the presence of the affected component). Table 1 number PH value Radix Codo nopsis Rhizoma Atractylod is Macrocep halae Pericarpium Citri Reticulata e Poria cocos (Schw.) Wolf Rhizoma Zingiberis S1 4.26 √ √ √ √ √ S2 4.27 √ √ √ - - S3 4.85 √ √ - √ - S4 5:15 √ √ - - √ S5 4.02 √ - √ √ - S6 4.32 √ - √ - √ S7 4.83 √ - - √ √ S8 3.78 - √ √ √ - S9 4:23 - √ √ - √ S10 4.84 - √ - √ √ S11 3.77 - - √ √ √
1. Alcoholic Liver Disease in Mice

Fifty-two male C57BL/6-type mice, eight weeks old, were pair-fed with liquid diet for one week so that they were adapting, while the control group was fed without alcohol. The mice were then divided into an alcohol-fed group and a pair-fed group (normal control group). The mice from the alcohol-fed group were fed Lieber-DeCarli liquid chow (high-fat alcoholic liquid chow) with an alcohol concentration of 1-5% (increasing 1-5% every day) every day, and the arbitrary feeding of the Mice fed a liquid diet at an alcohol concentration of 5% took 5 weeks. The pair-fed mice were fed a liquid diet (redistilled water (ddH ₂ O) as the liquid vehicle) of comparable calories as a normal control group for 5 weeks.

2nd treatment

At the beginning of the induction period, the mice were orally administered the vehicle (ddH2O) or the medicinal composition (PO) once a day (QD) for 35 days or 5 weeks. The volume of the dose was 12.3 mL/kg (body weight) and day 1 was designated as day 0. The design of the experiments is shown in Table 2. Table 2 group no . Number lining Treatment dose route of administration delivery frequency 1 4 liquid diet control group Carrier (ddH2O) 12.3 mL/kg PO QD x 35 2 4 liquid Lieber DeCarli nutrition Carrier (ddH2O) 12.3 mL/kg PO QD x 35 3 4 liquid Lieber DeCarli nutrition S1 12.3 mL/kg PO QD x 35 4 4 liquid Lieber DeCarli nutrition S2 12.3 mL/kg PO QD x 35 5 4 liquid Lieber DeCarli nutrition S3 12.3 mL/kg PO QD x 35 6 4 liquid Lieber DeCarli nutrition S4 12.3 mL/kg PO QD x 35 7 4 liquid Lieber DeCarli nutrition S5 12.3 mL/kg PO QD x 35 8th 4 liquid Lieber DeCarli nutrition S6 12.3 mL/kg PO QD x 35 9 4 liquid Lieber DeCarli nutrition S7 12.3 mL/kg PO QD x 35 10 4 liquid Lieber DeCarli nutrition S8 12.3 mL/kg PO QD x 35 11 4 liquid Lieber DeCarli nutrition S9 12.3 mL/kg PO QD x 35 12 4 liquid Lieber DeCarli nutrition S10 12.3 mL/kg PO QD x 35 13 4 liquid Lieber DeCarli nutrition S11 12.3 mL/kg PO QD x 35

In mice with alcoholic liver disease, the 11 medicinal compositions S1 - S11 were tested to assess their protection from alcoholic liver damage. The first group of animals was pair-fed liquid diet with the vehicle of (ddH ₂ O) as a normal control group. The 2nd group of animals were fed liquid Lieber-DeCarli diet with the carrier of (ddH ₂ O) as a disease control group. Groups 3 through 13 of animals were each fed Lieber-DeCarli liquid diet and medicinal composition S1-S11.

Out of 1 a significant reduction in their body weight is seen in the alcohol-fed mice. Compared to the vehicle control group (Group 2), no discernible change in body weight is visible in the treatment groups.

Out of 2 and 3 it can be seen that at the end of the study (day 34) the mean liver weight to body weight ratio is 5.78%, while in the normal control group (group 1) it is 3.55% (p<0.05); and that the mean kidney weight to body weight ratio is 1.35%, while in the normal control group (Group 1) it is 1.01% (p<0.05). It can therefore be seen that the liver weight and kidney weight to body weight ratios of the alcohol-fed mice are significantly increased.

Furthermore, referring to 2 It can be seen that after treatment in treatment group S1 (group 3), S2 (group 4), S3 (group 5), S5 (group 7), S6 (group 8) and S10 (group 12) the liver weight ratios to body weight are significantly reduced (p<0.05) compared to the vehicle control group (group 2).

3. Chemical measurement of serum

On day 0 and day 34, mice were fasted overnight prior to blood collection. Blood samples were taken 4 hours after the last administration for chemical analysis of the serum. Parameters for chemical analysis of serum include AST (aspartate aminotransferase), ALT (alanine aminotransferase), total cholesterol level (T-CHO), triglyceride level (TG) and glucose level (GLU), with AST, ALT, CHO and TG using Hitachi 7180 analyzer and GLU measured using a blood glucose meter.

Referring to 4 and 5 For example, chemical analysis of the blood on day 34 shows that compared to the normal control group (Group 1), the serum AST and ALT levels in the alcohol-fed mice are markedly elevated, with their AST levels being 122.5 ± 29.6 U/L and for the normal control group (Group 1) are 80.8 ± 3.5 U/L; their ALT levels are 49.7 ± 6.3 U/L and for the normal control group (Group 1) 33.9 ± 3.0 U/L (p<0.05). However, compared to the vehicle control group (Group 2), no major difference in AST and ALT levels is seen in the treatment groups.

Referring to 6 it can be seen that at the start of treatment (day 0) in treatment groups S1 (group 3), S3 (group 5), S5 (group 7), S7 (group 9) and S9 (group 11), total cholesterol (T- CHO) in the serum compared to the vehicle control group (group 2) is significantly increased (p < 0.05). However, at the end of the study (day 34) the level of T-CHO in the serum of the alcohol-fed mice was significantly increased (p<0.05) compared to the normal control group (group 1). However, compared to the vehicle control group (Group 2), no major increase in serum T-CHO levels is seen in the treatment groups.

Referring to 7 it can be seen that in the treatment group S2 (group 4), S3 (group 5), S5 (group 7), S6 (group 8) and S9 (group 11) the serum triglyceride (TG) level compared to the vehicle control group (group 2 ) is significantly reduced (p < 0.05). However, at the end of the study (day 34), compared to the normal control group (group 1), the serum TG level in the alcohol-fed mice was significantly reduced (p<0.05). However, compared to the vehicle control group (Group 2), no major change in serum TG levels is seen in the treatment groups.

Referring to 8th it can be seen that at the beginning of the treatment (day 0) in the treatment group S1 (group 3), S2 (group 4), S5 (group 7) the glucose level in the serum is significantly increased compared to the vehicle control group (group 2) (p < 0.05). However, at the end of the study (day 34) the serum glucose level of the alcohol-fed mice in treatment group S8 (group 10) was significantly reduced (p<0.05) compared to the vehicle control group (group 2).

4. Measurement of total cholesterol (T-CHO) and triglyceride levels in the liver

At the end of the study on day 34, liver tissue was collected and extracted with PBS. Total cholesterol (T-CHO) and triglyceride (TG) levels in the liver were evaluated using a Hitachi 7180 analyzer.

Referring to 9 and 10 total cholesterol (T-CHO) and triglyceride (TG) levels increase in the liver of alcohol-fed mice. In the treatment group S7 (group 9), S8 (group 10), S9 (group 11) and S11 (group 13), the level of T-CHO in the liver is significantly reduced (p < 0) compared to the vehicle control group (group 2). ,05). However, compared to the vehicle control group (group 2), the level of TG in the liver is significantly reduced in treatment group S8 (group 10) (p<0.05).

5. Measurement of hepatic enzymes

The level of glutathione peroxidase (GPx) in liver was measured by ELISA method and the results are shown in Table 3. Table 3 group no Treatment number Levels of lipids and enzymes in the liver (Day 34) T-CHO TG GPx (mg/g) (mg/g ) mU/mL 1 1 17.7 48.4 39.5 3 liquid diet control group 2 14.6 13.5 35.3 1st carrier 3 23:1 50.1 32.6 2 Water 4 18.0 11.2 20.4 7 12.3 mL/kg average value 18.4 30.8 31.9 8 PO, QD × 35 standard error of the mean 1.8 10.7 4.09 2 6 17.2 17.6 22.0 0 liquid nutrition from Lieber DeCarli Diet 7 20.2 64.5 24.8 2 carrier 8th 27.2 26.9 35.5 7 Water 9 17.7 55.2 32.3 7 12.3 mL/kg average value 20.6 41.0 28.6 9 PO, QD × 35 standard error of the mean 2.3 11.2 3:17 3 11 24.8 61.3 42.4 7 liquid nutrition from Lieber DeCarli Diet 12 22.7 44.8 30.7 0 S1 13 24.0 56.6 49.6 4 12.3 mL/kg 14 13.1 22.8 41:1 9 PO, QD × 35 average value 21:1 46.4 41.0 0 standard error of the mean 2.7 8.6 3.90 4 16 24.6 80.9 31.9 8 liquid nutrition from Lieber DeCarli Diet 17 17.9 32.6 39.2 8 S2 19 15.1 12.4 28.9 1 12.3 mL/kg 20 18.2 39.8 33.9 0 PO, QD × 35 average value 18.9 41.4 33.5 2 standard error of the mean 2.0 14.4 2:18 5 21 12.9 24.0 36.0 8 liquid nutrition from Lieber DeCarli Diet 22 13.4 21:9 40.6 8 S3 23 14.3 23.0 51.5 6 12.3 mL/kg 24 23.7 68.7 48.2 3 PO, QD × 35 average value 16.1 34.4 44.1 4 standard error of the mean 2.6 11.4 3.52 6 26 10.1 14.0 42.0 9 liquid nutrition from Lieber DeCarli Diet 28 20.0 46.4 43.8 8 S4 29 12.2 24.3 40.0 4 12.3 mL/kg 30 11.7 16.7 53.0 9 PO, QD × 35 average value 13.5 25.4 44.7 8 standard error of the mean 2.2 7.3 2.88 7 31 14.6 16.5 72.5 4th liquid nutrition from Lieber DeCarli Diet 32 17.1 18.2 55.0 1st S5 33 13.7 13.2 42.8 6 12.3 mL/kg 34 17.2 23.0 51.1 7 PO, QD × 35 average value 15.7 17.7 55.3 9 standard error of the mean 0.9 2.0 6.25 8th 36 13.7 25.1 47.2 1 liquid nutrition from Lieber DeCarli Diet 37 16.1 16.3 47.9 7 S6 38 15.3 17.8 61.5 4th 12.3 mL/kg 39 15.5 16.9 53.9 9 PO, QD × 35 average value 15.1 19.0 52.6 8 standard error of the mean 0.5 2.0 3.32 9 41 8.8 10.4 89.3 0 liquid nutrition from Lieber DeCarli Diet 42 12.2 12.1 64.4 8 S7 43 15.9 22.8 62.1 7 12.3 mL/kg 44 14.5 11.3 73.8 2 PO, QD × 35 average value 12.9† 14.1 72.4 4th standard error of the mean 1.6 2.9 6:16 10 45 15.5 9.8 60.6 4 liquid nutrition from Lieber DeCarli Diet 47 13.9 6.9 56.8 0 S8 48 10.1 14.6 60.5 1st 12.3 mL/kg 49 14.1 9.7 59.2 3 PO, QD × 35 average value 13.4† 10.3† 59.30 standard error of the mean 1.2 1.6 0.89 11 51 11.0 27.2 49.6 4 liquid nutrition from Lieber DeCarli Diet 52 16.2 18.7 46.4 4th S9 53 10.6 14.1 55.2 7 12.3 mL/kg 54 10.5 16.0 51.0 4th PO, QD × 35 average value 12:1† 19.0 50.6 0 standard error of the mean 1.4 2.9 1.83 12 56 14.4 27.9 74.9 7 liquid nutrition from Lieber DeCarli Diet 57 15.2 29.2 47.2 1 S10 58 14.4 23.2 54.7 5 12.3 mL/kg 60 15.9 19.9 35.9 5 PO, QD × 35 average value 14.9 25.0 53.2 2 standard error of the mean 0.4 2.1 8:21 13 61 15.4 13.7 57.4 4th liquid nutrition from Lieber DeCarli Diet 62 12.7 13.1 55.3 9 S11 63 11.0 14.6 68.8 3 12.3 mL/kg 64 14.7 8.9 63.3 3 PO, QD × 35 average value 13.4 12.6 61.2 5 standard error of the mean 1.0 1.3 3.03

6. Microscopic assessment

Tissue samples were collected at dissection of the mice and preserved in a 10% neutral buffered formalin (NBF) solution. The liver, kidney and intestinal tract were trimmed, embedded in paraffin, sectioned, stained with H (hematoxylin) and E (eosin) and viewed through a microscope (Leica DM2700M) checked.

6.1 Semi-quantitative evaluation of the disease focus of liver steatosis

The severity of the focus of hepatic steatosis under microscope is ranked as in Table 4, and the evaluation scores of the groups after treatment are in Tables 5 and 11 shown. Table 4 grade level 0 regular (0%) 1 minimal (< 10%) 2 easy (10 - 33%) 3 moderate (33 - 66%) 4 heavy (66 - 100%) Table 5 group no 1 2 3 4 Hepatic steatosis (mean value ± standard error of the mean) 1.00 ± 0.00 2.75±0.50 ^# 1.50 ± 1.29 2.00 ± 0.82 group no 5 6 7 8th Hepatic steatosis (mean value ± standard error of the mean) 2.25 ± 0.50 2.25 ± 0.50 1.25±0.50* 2.75 ± 0.50 group no 9 10 11 12 ( Hepatic steatosis (mean value ± standard error of the mean) 2.25 ± 0.96 2.50 ± 0.58 2.50 ± 0.58 1.50 ± 0.58 group no 13 Hepatic steatosis (mean value ± standard error of the mean) 3.00 ± 0.00
^#p <0.05 Group 2 vs Group 1
*p<0.05 Group 7 (with a weight ratio of Radix Codonopsis: Poria cocos (Schw.) Wolf: Pericarpium Citri Reticulatae of 14:20:14) vs. Group 2

Referring to 11 it can be seen that the treatment group S5 (group 7) had a significantly reduced score in the hepatic steatosis disease focus score of the Lieber-DeCarli liquid diet-fed mice compared to the vehicle control group (group 2) (p<0.05; unidirectional analysis of variance) having. This result therefore indicates that treatment group S5 (group 7) can provide increased protection of mice from alcohol-induced hepatic steatosis and ameliorate hepatic pathology in experimental mice with alcoholic liver disease.

6.2 Semi-quantitative evaluation of the histopathological findings

According to the literature disclosed in Toxicologic Pathology (Shackelfold et al., 2002), the severity of the microscopic pathological change (in the liver, kidney and intestinal tract) is graded as in Table 6, and the evaluating scores of the groups after treatment are in Table 7 shown. Table 6 grade level 0 normal 1 minimal (< 10%) 2 easy (10 - 39%) 3 moderate (40 - 79%) 4 hard (80 - 100%) Table 7 group no 1 2 3 4 5 Histopathological incidence Number of animals with histopathological findings / number of animals examined histopathologically liver Steatosis, multifocal, minimal to moderate 4/4 4/4 3/4 4/4 4/4 grade 1.00 ± 0.00 2.75±0.50 ^# 1.50 ± 1.29 2.00 ± 0.82 2.25 ± 0.50 Infiltration, mononuclear cells, focal, minimal 2/4 3/4 - 1/4 3/4 grade 0.50 ± 0.58 0.75 ± 0.50 - 0.25 ± 0.50 0.75 ± 0.50 kidney pathological change in kidney, slow progression, local, mild - - - 1/4 - grade - - - 0.50 ± 1.00 - Hyperplasia, acid-loving granulocyte, renal tubules, focal, minimal - - 1/4 - - grade - - 0.25 ± 0.50 - - tubular, renal tubules, focal, minimal to slight - - - - 1/4 grade - - - - 0.50 ± 1.00 Dilation, renal tubules, focal, minimal - - - - 1/4 grade - - - - 0.25 ± 0.50 intestinal tract denatured/necrotic, focal, minimal to slight - - - - 1/4 grade - - - - 0.50 ± 1.00 group no 6 7 8th 9 10 liver Steatosis, multifocal, minimal to moderate 4/4 4/4 4/4 4/4 4/4 grade 2.25 ± 0.50 1.25±0.50* 2.75 ± 0.50 2.25 ± 0.96 2.50 ± 0.58 Infiltration, mononuclear cells, focal, minimal 1/4 1/4 3/4 1/4 1/4 grade 0.25 ± 0.50 0.25 ± 0.50 0.75 ± 0.50 0.25 ± 0.50 0.25 ± 0.50 kidney tubular, renal tubules, focal, minimal to slight - 1/4 - - - grade - 0.25 ± 0.50 - - - Dilation, renal tubules, focal, minimal - - - 1/4 - grade - - - 0.25 ± 0.50 - mineralized, papillary tubules, focal, minimal - 1/4 - - - grade - 0.25 ± 0.50 - - - intestinal tract denatured/necrotic, focal, minimal to slight - - - - 1/4 grade - - - - 0.25 ± 0.50 group no 11 12 13 liver Steatosis, multifocal, minimal to moderate 4/4 4/4 4/4 grade 2.50 ± 0.58 1.50 ± 0.58 3.00 ± 0.00 Infiltration, mononuclear cells, focal, minimal 2/4 2/4 2/4 grade 0.50 ± 0.58 0.50 ± 0.58 0.50 ± 0.58
^#p <0.05 Group 2 vs Group 1
*p<0.05 Group 7 vs. Group 2

It can be seen from Table 7 that in the liver local minimal infiltration of mononuclear cells (2/4 of the male animals from group 1, 3/4 of the male animals from group 2, 1/4 of the male animals from group 4, 3 /4 of group 5 males, 1/4 of group 6 males, 1/4 of group 7 males, 3/4 of group 8 males, 1/4 of group 9 males, 1 /4 males from group 10, 2/4 males from group 11, 2/4 males from group 12 and 2/4 males from group 13). There was no statistical difference between the treatment groups and the vehicle control group (Group 2) in the severity of microscopic changes (p > 0.05; one-way analysis of variance).

It can be seen from Table 7 that in the kidney, slight local cortical pathological changes with slow progression (1/4 of male animals from group 4), minimal local cortical hyperplasia of acid-loving granulocytes in renal tubules (1/4 of male animals from group 3), minimal local cortical hyperplasia of acid-loving granulocytes in renal tubules (1/4 of males from group 5), minimal to slight local tubular renal tubules (1/4 of males from group 5 and 1/4 of males animals from group 7), minimal focal dilatation of the renal tubules (1/4 of males from group 5 and 1/4 of males from group 9), and minimal local mineralization of the papillary tubules (1/4 of males from group 7 ) to be observed. There was no statistical difference between the treatment groups and the vehicle control group (Group 2) in the severity of microscopic changes (p > 0.05; one-way analysis of variance).

It can be seen from Table 7 that minimal to slight focal denaturation/necrosis (1/4 of group 5 males and 1/4 of group 10 males) is observed in the intestinal tract. There was no statistical difference between the treatment groups and the vehicle control group (Group 2) in the severity of microscopic changes (p > 0.05; one-way analysis of variance).

The overall results indicate that the medicinal composition S5 can provide enhanced protection of mice from alcohol-induced hepatic steatosis and improve hepatic pathology in the above experimental mice.

7. Static Analysis

All values are expressed as mean ± standard deviation (S.D.) or standard error of the mean (SEM). An unpaired Student's t-test was used for the comparison between the normal group (Group 1) and the carrier group (Group 2), and a one-way ANOVA and a Dunnett test (Dunnett's test) were used for static analysis by comparison between the vehicle control group (Group 2) and the treatment groups (Group 3 to Group 13). If p has a value less than 0.05 (p < 0.05), the difference is considered to be statistically meaningful.

Example 2: Case Study of Effects of Medicinal Composition on Humans

A study involving 25 volunteers was conducted to determine the effect of the medicinal composition of the present invention on the increased BAC. The participants include 21 men and 4 women, ranging in age from 31 to 50. Table 8 shows the basic demographic details of the selected individual. Table 8. Demographic details of selected individual Volunteer (n=25) Characteristic n % Gender feminine 4 16 masculine 21 84 Old 25-30 1 4 31-40 10 40 41-50 9 36 > 51 5 20 Height (cm) Mean ± SEM 69.24±7.21 Body weight (kg) Mean ± SEM 73.22±9.56 level of education junior college 1 4 professional school 0 0 Bachelor 10 40 master 13 52 doctor 1 4 Body Mass Index (BMI) < 18.5 0 0 18:5-23:9 8th 32 24-26:9 11 44 27-29:9 5 20 30-34.9 1 4 = 35 0 0 Mean value ± SEM 25.50 ± 2.29 medical history intestinal tract disease 6 24 diabetes 0 0 gallstones 2 8th liver polyps 4 16 liver cyst 2 8th fatty liver disease 15 60

The medicinal composition (hereinafter referred to as "CGW3 preparation") contains the extract of a herbal mixture containing about 5-15% by weight Rhizoma Zingiberis, about 15-25% by weight Radix Codonopsis, about 25-35% by weight Poria cocos (Schw.) Wolf, about 15-25% by weight Pericarpium Citri Reticulatae, and about 10-20% by weight Rhizoma Atractylodis Macrocephalae.

• 1) Alkoholkonsum ohne Einnahme von CGW3-Zubereitung (Kontrolleinstellung)
• 2) Einnahme von 120 ml CGW3-Zubereitung 30 Minuten vor und 30 Minuten nach Alkoholkonsum.
• 3) Einnahme von 120 ml CGW3-Zubereitung einmal pro Tag für 15 Tage vor Alkoholkonsum, 30 Minuten vor und 30 Minuten nach Alkoholkonsum.

Examinations of each individual were made under each of 3 conditions:

• 1) Alcohol consumption without ingestion of CGW3 preparation (control setting)
• 2) Ingestion of 120 ml of CGW3 preparation 30 minutes before and 30 minutes after alcohol consumption.
• 3) Ingestion of 120 ml CGW3 preparation once per day for 15 days before alcohol consumption, 30 minutes before and 30 minutes after alcohol consumption.

1. (a) Nüchternheit-Feldtest, einschließlich des Finger-Nase-Tests, Zähltests (mit geschlossenen Augen) und Romberg-Gleichgewichtstests;
2. (b) ein selbst auszufüllender Fragebogen jeweils bei 1 Stunde, 2 Stunden und 24 Stunden nach Alkoholkonsum. Der Fragebogen bei 1 Stunde nach Alkoholkonsum zielte auf die vom Alkohol induzierten Syndrome des Katers, wie Schwindel, Fieber, Schwitzen, Kopfschmerzen, Bauchschmerzen, Durchfall, juckende Haut, Hautausschlag, und Bauchschmerzen, ab. Der Fragebogen bei 2 Stunden nach Alkoholkonsum zielte auf die vom Alkohol induzierten Zustände des Katers, wie undeutliches Sprechen, Änderung des Bewusstseinszustands, Verwirrtheit, unsicherer Gang, verschwommenes Sehen, und zittrige Hand, ab. Der Fragebogen bei 24 Stunden nach Alkoholkonsum zielte auf die folgenden, vom Alkohol induzierten Syndrome des Katers ab: schlechte Leistungsfähigkeit bei der Arbeit, Verminderung der Aufmerksamkeit oder des Gedächtnisses, Schwindel, Übelkeit, unwohles Gefühl im Bauch, Rückenschmerzen, Kopf- und Nackenschmerzen, trockene und unwohle Augen, Schlaflosigkeit und Schläfrigkeit;
3. (c) serologische Untersuchungen: Glukose-6-Phosphat-Dehydrogenase (G6PD), Alaninaminotransferase (ALT), Aspartataminotransferase (AST), γ-Glutamyltransferase (γ-GT), Kreatinin und Aldosteron.

Each male individual drank 147 ml of alcohol and each female individual 73.5 ml. After alcohol consumption, the following checks and assessments were performed by a neurologist:

1. (a) field sobriety test, including the finger-nose test, counting tests (eyes closed) and Romberg balance tests;
2. (b) a self-administered questionnaire at 1 hour, 2 hours and 24 hours after alcohol consumption. The questionnaire at 1 hour after alcohol consumption targeted alcohol-induced hangover syndromes such as dizziness, fever, sweating, headache, abdominal pain, diarrhea, itchy skin, rash, and abdominal pain. The questionnaire at 2 hours after alcohol consumption targeted alcohol-induced hangover conditions such as slurred speech, altered state of consciousness, confusion, unsteady gait, blurred vision, and trembling hand. The questionnaire at 24 hours after alcohol consumption was aimed at the following alcohol-induced hangover syndromes: poor performance at work, decreased attention or memory, dizziness, nausea, abdominal discomfort, back pain, headache and neck pain, dryness and uncomfortable eyes, insomnia and drowsiness;
3. (c) serological studies: glucose-6-phosphate dehydrogenase (G6PD), alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyltransferase (γ-GT), creatinine and aldosterone.

As in 12 and Table 9, the individuals who had ingested the CGW3 formulation 15 times prior to alcohol consumption performed much better than the control setting in the finger-nose test, counting test, and balance posture. In addition, the individuals who had once ingested the CGW3 preparation prior to alcohol consumption performed much better than the control setting in the counting test and in the steady state. The results indicate that ingestion of the CGW3 preparation at least once prior to alcohol consumption significantly improves performance in the non-standardized field sobriety test (including the finger-nose test, count test, and balance test). Table 9. Influence of the CGW3 preparation on the behavior in the fasting field test Taking CGW3 Odds Ratio (OR) + 95% CI Number at single (control = without CGW3- senior once only 15 times income) (n=25) (n=25) (n=25) only once 15 times successful ₁₈ 2,042 9,333 he finger 21 (84.00) 24 (96.00) (72.00) nose test (0.153-8.119) (1,052-82,774)* successful 9,333 9,333 he counting test 9 (36.00) 21 (84.00) 21 (84.00) (2,431-35,838)1 (2,431-35,838)1 equiv 6,000 4,333 posture 5 (20.00) g 15 (60.00) 13 (52.00) (1.693-21.261)1 (1.235-15.206)* *p<0.05, tp<0.01

As in Table 10 and in 13 until 15 demonstrated that ingestion of the CGW3 preparation once or 15 times prior to alcohol consumption reduces any hangover syndromes induced thereby. In particular, taking the CGW3 preparation 15 times before drinking alcohol not only relieves dizziness and confusion compared to the control setting, but also improves alertness and memory the next day. By taking the CGW3 preparation once before drinking alcohol, slurred speech and a change in consciousness are relieved compared to the control setting, and next-day work performance is also improved. Table 10. Effect of CGW3 preparation on alcohol-induced hangover syndromes CGW3 intake Odds Ratio (OR) + 95 CI action number of individuals once only 15 times (n=25) (n=25) (n=25) once only 15 times one hour after drinking alcohol dizziness 2.6 ± 1.26 1.96 ± 1.1 1.64 ± 0.86 0.318 (0.090-1.120) 0.196 (0.056-0.692)* hot flash and sweating 1.64 ± 0.81 1.44 ± 0.92 1.4 ± 0.65 0.421) (0.130-1.363) 0.510 (0.161-1.610) 0.444 Headache 1.56 ± 0.82 1.44 ± 0.87 1.32 ± 0.75 0.561 (0.164-1.918) (0.124-1.592) Abdominal pain and diarrhea itchy 1.4±0.87 1.32 ± 0.75 1.21 ± 0.51 1.000 (0.25-3.998) 0.762 (0.179-3.249) skin and rash 1.28±0.46 1.28 ± 0.61 1.12±0.33 0.643 (0.173-2.388) 0.351 (0.079-1.554) Stomach pain 1.24 ± 0.52 1.16 ± 0.47 1.12±0.44 0.545 (0.115-2.581) 0.348 (0.061-1.933) two hours after drinking alcohol slurred speech and change in consciousness 2.16 ± 1.07 1.64 ± 0.91 1.64 ± 0.91 0.306 (0.094-0.992)* 0.359 (0.111-, 1.161) confusion 2.08 ± 1.12 1.68 ± 1.07 1.44 ± 0.77 0.375 (0.120-1.176) 0.265 (0.082-0.855)* 0.434 unsteady walk 2.04 ± 0.93 1.68 ± 0.85 1.64 ± 0.81 0.434 (0.138-1.372) (0.138-1.372) 0.375 blurred vision 1.56 ± 0.82 1.4 ± 0.91 1.28 ± 0.61 0.474 (0.140-1.601) (0.106-1.329) 0.457 shaky hand 1.24 ± 0.6 1.2±0.5 1.08±0.28 1.000 (0.22-4.536) (0.076-2.755) 24 hours after alcohol consumption Decreased attention or memory 1.72 ± 0.79 1.44 ± 0.71 1.28 ± 0.54 0.434 (0.138-1.371) 0.291 (0.087-0.975)* poor performance at work dizziness, 1.72±0.84 1.24 ± 0.52 1.4 ± 0.76 0.271 (0.077-0.95)* 0.421 (0.130-1.363) Nausea and discomfort in the abdomen 1.88 ± 1.09 1.48±0.87 1.4 ± 0.76 0.434 (0.138-1.371) 0.359 (0.111-1.161) loss of appetite 1.8±1.12 1.6 ± 0.91 1.52 ± 0.77 0.848 (0.276-2.611) 0.848 (0.276-2.611) Back and neck pain 1.68±0.9 1.4 ± 0.65 1.36±0.7 0.510 (0.161-1.610) 0.421 (0.130-1.363) dry and uncomfortable eyes 1.52 ± 0.77 1.36 ± 0.76 1.32 ± 0.63 0.561 (0.164-1.918) 0.561 (0.164-1.918) Drowsiness *= P<0.05 1.32 ± 0.63 1.44 ± 0.82 1.4 ± 0.65 0.510 (0.161-1.610) 0.370 (0.117-1.172)

Table 11 and 16 - 18 show the influence of the CGW3 preparation on the liver and kidney function tests as well as the G6PD level. Ingestion of the CGW3 preparation once prior to alcohol consumption significantly reduces serum G6PD and γ-GT levels compared to the control setting. By taking the CGW3 preparation 15 times before alcohol consumption, the serum ALT and AST levels are significantly reduced and at the same time it is observed that the serum creatinine level tends to decrease. Table 11 Effect of CGW3 preparation on liver and kidney function tests no alcohol consumption once only (n=25) (n=25) average avg p-value worthwhile S.E.M t S.E.M glucose-6-phosphate < Dehydrogenase (G6PD) (U/gHb) 13.06 2.22 12:21 2.2 0.000 1† Aspartate aminotransferases (AST) (U/L) 27.64 6.84 27.84 7.33 0.699 Alanine Aminotransferase (ALT) (U/L) 32 16.99 30.52 15:16 0.896 γ-Glutamyltransferase 0.028 (γ-GT) (U/L) 32.88 30.87 28.96 24.62 * Creatinine (mg/dL) 0.97 0.16 0.97 0.14 0.824 Aldosterone (pg/mL) 9.42 5.18 9:16 5.31 0.323 *p<0.05, †p<0.01

Example 3: Study of influencing medicinal composition in vivo

The effects of CGW3 preparation on intestinal tract barrier and glomerulus were evaluated.

1. 1. Übliches Kontrollfutter: Die Mäuse wurden über 4 Wochen durch Sondennahrung mit Lieber-DeCarli-Nahrung (221,78 g von Lieber-DeCarli-Standardnahrungspulver gemischt in 1 L destilliertes Wasser) gefüttert. Während der Woche vor dem üblichen Kontrollfutter und während des gesamten Untersuchungsvorgangs wurden sie oral durch Sondennahrung mit 12,3 ml destilliertem Wasser pro kg Körpergewicht pro Tag versorgt.
2. 2. Flüssiges alkoholisches Futter: Die Mäuse wurden gemäß dem 2016 von der chinesisch-taiwanesischen Lebensmittel- und Arzneimittel-Überwachungsbehörde offenbarten Verfahren zur Beurteilung der Wirksamkeit von gesunden Lebensmitteln in der Leber (Evaluation Method of Liver Health Care Efficacy of Healthy Food) über 4 Wochen durch Sondennahrung mit der alkoholischen Lieber-DeCarli-Nahrung (132.18 g alkoholische Standard-Lieber-DeCarli-Nahrung und 67 ml 95%-iger Alkohol in 933 ml destilliertem Wasser) gefüttert, um die Beschädigung des Darmtrakts und der Niere zu induzieren. Während der Woche vor dem flüssigen alkoholischen Futter und während des gesamten Untersuchungsvorgangs wurden sie oral durch Sondernahrung mit 12,3 ml destilliertem Wasser pro kg Körpergewicht pro Tag gefüttert.
3. 3. Flüssiges alkoholisches Futter + 4,1 ml CGW3-Zubereitung pro kg Körpergewicht pro Tag: Die Mäuse wurden über 4 Wochen durch Sondennahrung mit der alkoholischen Lieber-DeCarli-Nahrung gefüttert. Während der Woche vor dem flüssigen alkoholischen Futter und während des gesamten Untersuchungsvorgangs wurden sie oral durch Sondennahrung einmal pro Tag über insgesamt 5 Wochen mit 4,1 ml CGW3-Zubereitung pro kg Körpergewicht pro Tag (äquivalent zu 0,33 mg/kg menschliches Körpergewicht pro Tag) versorgt.
4. 4. Flüssiges alkoholisches Futter + 12,3 ml CGW3-Zubereitung pro kg Körpergewicht pro Tag: Die Mäuse wurden über 4 Wochen durch Sondennahrung mit der alkoholischen Lieber-DeCarli-Nahrung gefüttert. Während der Woche vor dem flüssigen alkoholischen Futter und während des gesamten Untersuchungsvorgangs wurden sie oral durch Sondennahrung einmal pro Tag über insgesamt 5 Wochen mit 12,3 ml CGW3-Zubereitung pro kg Körpergewicht pro Tag (äquivalent zu 1 mg/kg menschliches Körpergewicht pro Tag) versorgt.
5. 5. Flüssiges alkoholisches Futter + 36,9 ml CGW3-Zubereitung pro kg Körpergewicht pro Tag: Die Mäuse wurden über 4 Wochen durch Sondennahrung mit der alkoholischen Lieber-DeCarli-Nahrung gefüttert. Während der Woche vor dem flüssigen alkoholischen Futter und während des gesamten Untersuchungsvorgangs wurden sie oral durch Sondennahrung einmal pro Tag über insgesamt 5 Wochen mit 36,9 ml CGW3-Zubereitung pro kg Körpergewicht pro Tag (äquivalent zu 3 mg/kg menschliches Körpergewicht pro Tag) versorgt.

For this study, 8-10 week old male mice of type C57BL/6 with a body weight of 20 g (commercially available from Animal Center, Taiwan, China, and fed in Animal Center of Changgeng University, IACUC No. CGU108-009) were used. . The study includes 5 study groups, each with 10 mice.

1. 1. Common Control Chow: Mice were tube-fed Lieber-DeCarli formula (221.78 g of Lieber-DeCarli standard formula powder mixed in 1 L of distilled water) for 4 weeks. During the week prior to the usual control chow and throughout the study period, they were orally gavaged at 12.3 ml distilled water per kg body weight per day.
2. 2. Liquid alcoholic feed: The mice were treated according to the Evaluation Method of Liver Health Care Efficacy of Healthy Food disclosed by the China-Taiwan Food and Drug Administration in 2016 for 4 weeks gavage-fed with the Lieber DeCarli alcoholic formula (132.18 g of standard Lieber DeCarli alcoholic formula and 67 ml of 95% alcohol in 933 ml of distilled water) to induce damage to the intestinal tract and kidney. During the week prior to the liquid alcoholic chow and throughout the study procedure, they were orally fast-fed at 12.3 ml distilled water per kg body weight per day.
3. 3. Liquid alcoholic chow + 4.1 ml CGW3 preparation per kg body weight per day: Mice were tube-fed the Lieber-DeCarli alcoholic chow for 4 weeks. During the week prior to the liquid alcoholic chow and throughout the study procedure, they were orally gavaged once per day for a total of 5 weeks with 4.1 mL of CGW3 preparation per kg body weight per day (equivalent to 0.33 mg/kg human body weight per day) supplied.
4. 4. Liquid alcoholic chow + 12.3 ml CGW3 preparation per kg body weight per day: Mice were gavaged with the Lieber-DeCarli alcoholic chow for 4 weeks. During the week prior to the liquid alcoholic chow and throughout the study process, they were orally gavaged once per day for a total of 5 weeks at 12.3 mL of CGW3 preparation per kg body weight per day (equivalent to 1 mg/kg human body weight per day). provided.
5. 5. Liquid alcoholic chow + 36.9 ml CGW3 preparation per kg body weight per day: Mice were gavaged with the Lieber-DeCarli alcoholic chow for 4 weeks. During the week prior to the liquid alcoholic chow and throughout the study process, they were orally gavaged once per day for a total of 5 weeks at 36.9 mL of CGW3 preparation per kg body weight per day (equivalent to 3 mg/kg human body weight per day). provided.

After the administration of the CGW3 preparation for 5 weeks, the protection of the intestinal tract barrier and the glomerulus by the CGW3 preparation was evaluated.

pathological examination

After sacrificing the mice, the empty intestine and kidney tissue were fixed in a 10% formalin solution and stained according to the hematoxylin-eosin approach. Staining result: The cell nuclei were stained blue and the cytoplasm and intercellular substances were stained red.

Results:

The comparison of Figure B's 19 with the figure of the mice fed with the usual control chow (Figure A of the 19 ) shows that the jejunal villi of mice fed the liquid alcoholic chow is damaged. Jejunal villus damage was reversed or facilitated by regular feeding of the CGW3 preparation ( to E der 19 ).

The comparison of Figure B's 20 with the figure of the mice fed with the usual control chow (Figure A of the 20 ) shows that the glomeruli of the mice fed the liquid alcoholic chow are damaged. Glomerulus is a tissue in the kidney, and the original urine produced by the filtration of the glomerulus is surrounded by Bowman's capsules. The main purpose of the glomeruli is to filter blood plasma to remove waste and generate urine. Damage to the glomerulus was reversed or facilitated by regular feeding of the CGW3 preparation ( to E der 20 ).

Example 4: Case study of medicinal composition after consuming wine

Two adult volunteers who drank 250 mL of wine were designated as a control group, and an experimental group 1 containing medicinal composition S5 containing Radix Codonopsis, Poria cocos (Schw.) Wolf and Pericarpium Citri Reticulatae (the weight ratio of Radix Codonopsis, Poria cocos (Schw.) Wolf and Pericarpium Citri Reticulatae is 25 - 35% : 30 - 50% : 25 - 35%) as well as 250 mL of wine, and a test group 2, which used a medicinal composition with Radix Codonopsis, Poria cocos (Schw .) Wolf and Pericarpium Citri Reticulatae Viride (the weight ratio of Radix Codonopsis, Poria cocos (Schw.) Wolf and Pericarpium Citri Reticulatae Viride is 25 - 35% : 30 - 50% : 25 - 35%) and 250 mL of wine . To determine the difference between adding Pericarpium Citri Reticulatae and Pericarpium Citri Reticulatae Viride to the medicinal composition in terms of alcohol concentration reduction, alcohol concentrations were determined using a professional electrochemical alcohol meter (HOHOGA-AT576-AlcoREAL type) from Hanxun Technologies. The average alcohol concentrations of two volunteers are shown in Table 12. Table 12 Control group (consumption of 250 mL of wine) Experimental group 1 (consumption of 250 mL of wine + medicinal composition) (Radix Codonopsis + Poria cocos (Schw.) Wolf + Pericarpium Citri Reticulatae) Experimental group 2 (consumption of 250 mL of wine + medicinal composition) (Radix Codonopsis + Poria cocos (Schw.) Wolf + Pericarpium Citri Reticulatae Viride) Before drinking wine alcohol concentration (mg/L) 0 0 0 5 minutes after consuming wine alcohol concentration (mg/L) 0.644 0.65 0.6 30 minutes after consuming wine alcohol concentration (mg/L) 0.108 0.091 0.097 50 minutes after consuming wine alcohol concentration (mg/L) 0.074 0.071 0.10 70 minutes after consuming wine alcohol concentration (mg/L) 0.25 0.039 0.087 90 minutes after consuming wine alcohol concentration (mg/L) 0.095 0 0.077 110 minutes after consuming wine alcohol concentration (mg/L) 0.075 0 0.066 130 minutes after consuming wine alcohol concentration (mg/L) 0.042 - 0.057 150 minutes after consuming wine alcohol concentration (mg/L) 0.039 - 0.039

It can be seen from Table 12 that the alcohol concentration measured after 30 minutes for experimental group 1 was lower than that of the control group and experimental group 2. In addition, after 90 minutes, the alcohol concentration had become zero for test group 1, i. H. she could not be detected by the breathalyzer. It was found from the above results that a medicinal composition containing Pericarpium Citri Reticulatae according to the present invention had a better anti-hangover effect than a composition containing Pericarpium Citri Reticulatae Viride and could reduce the alcohol concentration to 0 in a shorter time.

QUOTES INCLUDED IN DESCRIPTION

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Patent Literature Cited

• US4938949 [0038]

Claims (13)

Use of a medicinal composition in the manufacture of a medicine for treating or reducing the effects of alcohol consumption on an individual, the medicinal composition comprising: (1) an herbal mixture containing: radix codonopsis; Poria cocos (Schw.) wolf; and Pericarpium Citri Reticulatae, and (2) a pharmaceutically acceptable carrier. use after claim 1 , where the weight ratio of Radix Codonopsis : Pericarpium Citri Reticulatae : Poria cocos (Schw.) Wolf in the herbal mixture is 25-35% : 25-35% : 30-50%. use after claim 1 wherein the herbal mixture further comprises Rhizoma Zingiberis and Rhizoma Atractylodis Macrocephalae. use after claim 3 , wherein the herbal mixture contains 5-15% by weight Rhizoma Zingiberis, 15-25% by weight Radix Codonopsis, 25-35% by weight Poria cocos (Schw.) Wolf, 15-25% by weight Pericarpium Citri Reticulatae, and 10-20% by weight of Rhizoma Atractylodis Macrocephalae. use after claim 1 until 4 , wherein the medicinal composition is taken before drinking alcohol. use after claim 1 until 4 wherein the effect on alcohol consumption is selected from the group consisting of: blood alcohol concentration syndromes and hangover. Medicinal composition comprising: (1) an herbal mixture containing: radix codonopsis; Poria cocos (Schw.) wolf; and Pericarpium Citri Reticulatae, and (2) a pharmaceutically acceptable carrier. Medicinal composition after claim 7 , where the weight ratio of Radix Codonopsis : Pericarpium Citri Reticulatae : Poria cocos (Schw.) Wolf in the herbal mixture is 25-35% : 25-35% : 30-50%. Medicinal composition after claim 7 wherein the herbal mixture further comprises Rhizoma Zingiberis and Rhizoma Atractylodis Macrocephalae. Medicinal composition after claim 9 , wherein the herbal mixture contains 5-15% by weight Rhizoma Zingiberis, 15-25% by weight Radix Codonopsis, 25-35% by weight Poria cocos (Schw.) Wolf, 15-25% by weight Pericarpium Citri Reticulatae, and 10-20% by weight of Rhizoma Atractylodis Macrocephalae. Use of the medicinal composition after claim 7 until 10 in the manufacture of a medicine for treating or reducing inflammation of liver cells and accumulation of fat. Use of the medicinal composition after claim 7 until 10 in the manufacture of a medicine for the treatment or reduction of damage to the function of the mucous membrane of the small intestine or intestines. Use of the medicinal composition after claim 7 until 10 in the manufacture of a medicine for the treatment or reduction of damage to the glomerulus or function of the kidney.

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