KR102057923B1 - the herb extraction composite with the function of anti-hyperlipidemia - Google Patents

Abstract

The present invention relates to a natural composition having antihyperlipidemic effect, and more particularly, to a composition having antihyperlipidemic effect, which has no side effects using natural herbs such as persimmon soup, licorice, and deficiency.
The present invention is a natural composition having antihyperlipidemic effect extracted by mixing the mixture of persimmon soup, licorice, missing name, Angelica, Sansa, Saengjihwang, Shiho, Injinho, Chajeon, Shouo, Red ginseng,
It provides a composition having an antihyperlipidemic effect of a mixture of fermented antler extract.
In addition, the natural composition of the present invention is 100 parts by weight of persimmon guk 80 to 120 parts by weight, 80 to 120 parts by weight of the deficiency, Angelica 80 to 120 parts by weight, hawthorn 80 to 120 parts by weight, raw turmeric 80 to 120 parts by weight, Shiho 80-120 parts by weight, Injin-ho 80-120 parts by weight, cha-cha 80-120 parts by weight, 80 ~ 120 parts by weight of sewage, 80-120 parts by weight of red ginseng extract composition characterized in that the antihyperlipidemic effect To provide.
In another aspect, the present invention provides a pharmaceutical composition that is effective in the prevention and treatment of hyperlipidemia, including the antihyperlipidemic composition.

Description

The herb extraction composite with the function of anti-hyperlipidemia

The present invention relates to a natural composition having an antihyperlipidemic effect, and more particularly, to a composition having an antihyperlipidemic effect, which has no side effects using natural herbs such as persimmon soup, licorice, and deficiency.

Hyperlipemia refers to a condition in which lipids such as cholesterol and triglycerides are not properly metabolized, resulting in a large amount of lipids in the blood. In other words, hyperlipidemia refers to serum lipids such as cholesterol, triglycerides, phospholipids and free fatty acids. One or more specific states of elevated levels, especially when measured clinically, high serum cholesterol levels above 200 mg / dL is called hypercholesterolemia, fasting triglyceride levels of 150 mg / The case of dL or more is called hypertriglyceridemia.

On the other hand, hyperlipidemia can be divided into hereditary hyperlipidemia and secondary hyperlipidemia. Hereditary hyperlipidemia is caused by abnormalities related to absorption, synthesis, and regulation of lipid components, and if there are patients with hyperlipidemia in the family, the incidence of genetic hyperlipidemia is high. In addition, secondary hyperlipidemia may occur due to acquired excessive animal fat intake, carbohydrate intake, obesity, drugs, etc., and is accompanied by diseases such as hypothyroidism, jaundice, nephrotic syndrome, and diabetes mellitus.

Cholesterol, one of the causes of hyperlipidemia, is a component of cell membranes, which is involved in the fluidity of cell membranes. In other words, the lack of cholesterol in the body weakens the cell membranes, and conversely, the cell membranes stiffen and cell activities decrease. It is a raw material for making bile acids that help absorption, and is also used for the synthesis of various steroid hormones to maintain the function of the body.

On the other hand, triglycerides, another cause of hyperlipidemia, are called triglycerides and are used as cell membrane components and energy sources in the body. Ingestion of triglycerides, such as triglycerides, increases obesity, and the triglycerides absorbed in the body may accumulate abnormally in the liver to form fatty livers. Absorbed carbohydrates are converted to fatty acids, a component of the triglyceride structure in the liver and adipose tissue, increasing the amount of triglycerides in the body.

Cholesterol and triglycerides, which perform these functions in the body, are delivered to each cell through the blood. However, because cholesterol and triglycerides are water insoluble, they are supplied to the blood in the form of proteins associated with them for delivery through the blood. The form in which the lipid component and the protein are combined is called a lipoprotein, and a polar phospholipid and free cholesterol surround the surface of the lipid component by using a hydrophobic cholesterol ester and a triglyceride as a nucleus. apoprotein) has a combined form.

These lipoproteins are classified into chylomicrons, ultra low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL).

According to the knowledge in the art, triglycerides are present in the blood in the form of chylomicrons and ultra low density lipoproteins, and cholesterol is present in the form of low density lipoproteins and high density lipoproteins. When too low density lipoprotein is present in the blood, the lipoprotein is deposited on the blood vessel wall inside the artery, where inflammatory cells such as leukocytes gather and smooth muscle cells proliferate, causing arteriosclerosis such as coronary arteriosclerosis. When triggered, blood vessels become narrower, their elasticity decreases, and their blood flow decreases, reducing the supply of oxygen and nutrients to many organs, leading to ischemic cardiovascular disease or stroke.

On the other hand, high-density lipoproteins take cholesterol from tissues and send it to the liver to break down, and when cholesterol-containing high-density lipoproteins are reduced, it has been reported that atherosclerosis occurs more easily.

As can be seen, in order to treat hyperlipidemia that causes atherosclerosis, the goal is to reduce the content of cholesterol and triglycerides in the blood. For example, the goal of treating hyperlipidemia in the clinic, for example, cholesterol and triglyceride values It is to keep all less than 200mg / ㎗.

The choice of treatment is determined by the level of cholesterol in the blood, for example, when the cholesterol level is 200 ~ 250 ㎎ / 주로 mainly diet, 250 ~ 300 ㎎ / 겸 combination of diet and drug therapy, When 300 mg / dl or more, thorough lipid-lowering drug administration is required.

On the other hand, the method for reducing the content of cholesterol and triglycerides in the blood can be classified into two types.

The first is to reduce the body's absorption of fat, which is usually done by eating foods that are low in fat, especially cholesterol and triglycerides. It is very difficult. Therefore, such a diet can only be effective in combination with drug therapy.

As one of these drug therapies, there is a method of inhibiting the activity of pancreatic lipases. Triglycerides themselves cannot be absorbed into the body through the intestinal wall, and are produced by pancreatic lipase, an enzyme secreted by the pancreas. After being absorbed into the body in the form of two free fatty acids, the triglyceride is absorbed into the body by combining these decomposition products in the body. Therefore, if the activity of the pancreatic lipase can be inhibited, The amount of absorption into the body can be reduced to reduce blood triglycerides. Therefore, many studies have been conducted in the art to find a substance capable of inhibiting the activity of pancreatic lipase.

On the other hand, another method of reducing blood fat component is to control metabolism related to synthesis and degradation of fat component.

According to common knowledge in the art, cholesterol metabolism, in particular synthetic metabolism, is known to be inhibited by reducing the activity of HMG CoA reductase. As an enzyme involved in the production of melateons, when the amount of cholesterol in the body is large, the activity of this enzyme is inhibited through a feedback action, thereby reducing the biosynthesis of cholesterol in the body.

In addition, it has been reported that blood cholesterol levels are rapidly increased in individuals mutated by this enzyme. Thus, substances that inhibit the activity of HMG CoA reductase may be used for the treatment of hyperlipidemia and arteriosclerosis, and the like in the art. Many studies have been conducted to find.

In related prior art, Patent No. 10-1854367 (antihyperlipidemic composition comprising ginseng berry extract) consists of "ginseng berry extract and fermented antler extract, and the ginseng berry extract and fermented antler extract are mixed in a weight ratio of 7: 3. , The ginseng berry extract is prepared by alcohol extraction or hot water extraction, the fermented antler extract is characterized in that fermented antler extract prepared by alcohol extraction or hot water extraction crushed antler using a Bacillus subtilis strain Antihyperlipidemic composition ".

The above-described prior art has side effects that are toxic to the liver and kidneys, and also the prior art has a lack of anti-hyperlipidemic effect, the present invention is natural with excellent anti-hyperlipidemic efficacy without toxicity to the liver and kidney. It is intended to provide a composition.

The present invention to solve the above object and demands,

Natural composition with antihyperlipidemic effect, which is a mixture of persimmon soup, licorice, deficiency, Angelica, Sansa, Saenghwanghwang, Shiho, Injinho, Chajeon, Shouao, and red ginseng,

It provides a composition having an antihyperlipidemic effect of a mixture of fermented antler extract.

In addition, the present invention, the natural composition is 100 parts by weight of persimmon soup 80 to 120 parts by weight, 80-120 parts by weight of the deficiency, 80-120 parts by weight, Angelica 80-120 parts by weight, 80-120 parts by weight of raw turmeric 80-120 parts by weight, Injin Ho 80-120 parts by weight, 80-120 parts by weight of chajeon, 80-120 parts by weight of sewage, 80-120 parts by weight of red ginseng extract composition characterized in that the antihyperlipidemic effect To provide.

In another aspect, the present invention provides a pharmaceutical composition that is effective in the prevention and treatment of hyperlipidemia, including the antihyperlipidemic composition.

The anti-hyperlipidemic composition according to the present invention is not toxic to the liver and kidney, but the anti-hyperlipidemic effect is excellent bar, it shows a significant effect on the prevention and treatment of hyperlipidemia.

1 to 19 is a table showing the results of animal experiments of the antihyperlipidemic composition according to the present invention.

Hereinafter, the present invention will be described in detail with reference to the drawings.

The present invention provides a natural composition extracted from a mixture of persimmon soup, licorice, the deficiency, Angelica, Sansa, Saenghwanghwang, Shiho, Injinho, Chajeon, Sewao, Red ginseng.

The present invention is preferably 100 parts by weight of persimmon licorice 80-120 parts by weight, 80-120 parts by weight of deficiency, 80-120 parts by weight of Angelica, 80-120 parts by weight of hawthorn, 80-120 parts by weight of raw sulfur, 80-120 It provides a natural composition extracted by mixing 80 parts by weight, 80 to 120 parts by weight, 80 to 120 parts by weight, 80 to 120 parts by weight of sewage, 80 to 120 parts by weight of red ginseng.

The present invention provides a natural composition in which the raw materials mixed in the above weight parts are extracted by mixing purified water or water and heating.

The present invention can be obtained by mixing 50 to 2000 parts by weight of purified water or water to 100 parts by weight of the raw material mixed in the above-mentioned parts by weight to obtain an extract.

The present invention is also mixed with 50 to 2000 parts by weight of distilled water to 100 parts by weight of the raw material and reflux extraction for 2 to 4 hours and then the filtrate is extracted by concentrating under reduced pressure with a rotary vacuum evaporator.

The concentrated solution is lyophilized with a freeze dryer to obtain a powder obtained.

The present invention provides a composition having an antihyperlipidemic effect by mixing fermented antler extract with the natural composition described above.

The present invention provides an antihyperlipidemic composition of 80 to 120 parts by weight of the fermented antler extract, preferably 100 parts by weight, to 100 parts by weight of the natural composition.

The present invention provides a pharmaceutical composition that is effective in the prevention and treatment of hyperlipidemia, comprising the composition having the above antihyperlipidemic effect.

Fermented antler extract of the present invention can be used a fermented antler extract prepared conventionally.

In one embodiment of the fermented antler extract, a deer antler medium (Bacillus P-92 strain) is made by sterilizing by adding 100 parts by weight of a moderately cut antler (New Zealand deer antler) and 5 to 40 times distilled water of this weight to sterilize it. After culturing for 1 to 7 days by culturing in sterilized filtrate can be prepared as a fermented antler extract.

Deer antler inoculated with lactic acid bacteria is 26 to 40 ℃, preferably 28 to 35 ℃, more preferably 30 to 32 ℃, 5 to 72 hours, preferably 10 to 60 hours, more preferably 24 to 48 hours Fermentation is preferred.

The present invention also provides an antihyperlipidemic pharmaceutical composition comprising the antihyperlipidemic composition described above.

<Example>

I. Sample manufacturing

1. Sample Extraction

(1) 10 g of persimmon soup, 10 g of licorice, 10 g of gleaner, 10 g of Angelica ginseng, 10 g of hawthorn, 10 g of raw turmeric, 10 g of shiho, 10 g of Injinho, 10 g of tea, 10 g of sewage, 10 g of red ginseng and 10 g of red ginseng After the reflux extraction for 3 hours to put the filtrate was concentrated under reduced pressure with a rotary vacuum evaporator to prepare a natural composition.

29.53 g (yield 23.81%) of the natural composition powder obtained by freeze-drying the concentrated natural composition solution with a freeze dryer were stored in an cryogenic freezer (-80 ° C).

A lactic acid bacterium (Bacillus P-92 strain) was implanted into a sterile medium made by sterilizing 100 g of antler (New Zealand antler) appropriately in distilled water and 1,500 g of distilled water. Was concentrated under reduced pressure with a rotary vacuum evaporator.

22 g of the fermented antler powder obtained by freeze-drying the concentrated fermented antler extract with a freeze dryer was stored in an cryogenic freezer (-80 ° C).

(2) The above-mentioned natural composition powder and fermented antler powder were mixed in the same amount (mixture and fermentation cervi parvum cornu hereinafter, MFC ) and diluted in distilled water to the concentration required for the experiment and used in animal experiments.

2. Specification and Management of Laboratory Animals

(1) SD rats (4 weeks old, males, 60-100 g) used for this experiment were purchased from Samtaco (Korea). The experimental animals received 300 g of normal feed (ENVIGO CO., UK) and sufficient water every week for 12 weeks of hyperlipidemia and 4 weeks of experiment. The control and sample groups received 300 weeks of hyperlipidemia every week. High-cholesterol diets (Research Diets Inc., USA) and fructose (Danisco Co., Finland) of grams were dissolved in distilled water at 25% concentration. The composition of normal and high cholesterol diets is shown in Table 2. The conditions of the animal breeding room were the conventional system, 22 ± 2 ℃, and 12 hours of the day were illuminated with 200-300 Lux, and 12 hours were blocked all the light. This experiment was approved in accordance with the animal ethics regulations with the approval of the Daejeon University Animal Experiment Ethics Committee (approval number DJUARB2017-035).

(2) reagent And devices

Reagents used were formaldehyde (Sigma Co., U.S.A.) and the like. The instrument used was Autoclave (Sanyo Co., Japan), Vortex mixer (Vision scientific Co., Korea), Centrifuge (Sigma Co., U.S.A.), Light Microscope (Carl Zeiss, Co., Germany).

3. How to

(1) sample administration

After 12 weeks of hyperlipidemia-induced hypercholesterol induction, the normal group received no treatment, and the negative control group received oral distilled water. In the positive control group, 15.6 g of the adult dose of cholestyramine, an anti-arterial drug, was based on 60 kg of adult body weight, and the experimental group was 600 g of the experimental animal body weight based on MFC of 200, 400 mg / kg. Sample doses were calculated and administered orally once daily at 10 am for 4 weeks.

(2 ) Separation and storage of serum and protein

After completion of the experiment, blood was collected by cardiac puncture, and the blood was solidified at room temperature for 30 minutes, centrifuged at 3,000 rpm for 15 minutes to separate serum, and stored in an ep tube as much as the capacity for the biomarker measurement kit. Also, the extracted liver tissue was washed with PBS, 1 ml of PBS per 0.1 g was added, and after sonication, centrifugation was performed at 3,000 rpm for 5 minutes, and the supernatant was stored in an ep tube as much as the capacity for the biomarker measurement kit. The ep tube was stored in a cryogenic freezer (-80 ℃).

 (3) liver and renal function measurement

After the end of the experiment, blood was collected by cardiac puncture and solidified at room temperature for 30 minutes, followed by centrifugation at 3,000 rpm for 15 minutes, and serum was separated to determine liver function indicators (AST, ALT, ALP, LDH), renal function indicators (BUN, creatinine) were submitted to KPNT for examination.

 (4) lipid metabolism in the blood Biomarker  Measure

  1) TC, HDL-C, LDL-C, TG

100 μl of serum and standard was separated into a 96 well plate and reacted at 37 ° C. for 90 minutes. After the reaction, 100 μl of detection antibody was added and reacted again at 37 ° C. for 60 minutes and washed three times using a washing buffer. After washing, 100 μl of HRP cunjugate was added and reacted at 37 ° C. for 30 minutes. After washing, 90 μl of substrate reagent was added and reacted at 37 ° C. for 15 minutes, and 50 μl of stop solution was added to absorb absorbance at 450 nm through ELISA reader. The measured value was expressed as an absolute value based on a standard curve.

2) VLDL

100 μl of serum and standard was separated into a 96 well plate and reacted at 37 ° C. for 90 minutes, and then washed three times using washing buffer. After washing, 100 μl of detection antibody was added and reacted again at 37 ° C. for 60 minutes and washed three times. Then, 100 μl of HRP-streptavidin cunjugate was added and reacted at 37 ° C. for 30 minutes, followed by washing. After reacting for 15 minutes at 50 μl and adding a 50 μl stop solution, the absorbance at 450 nm was measured using an ELISA reader, and the absolute value was expressed based on a standard curve.

 (5) arteriosclerosis index (AI) and cardiovascular risk index ( CRF )

Atherosclerosis index (Atherogenic Index, AI) was calculated using the formula of Fiordaliso AI = ([Total-C]-[HDL-C]) / [HDL-C]. In addition, the cardiovascular risk index (Cardiac Risk Factor, CRF) was calculated using the Rosenfeld calculation method, CRF = [Total-C] / [HDL-C].

(6) lipid metabolism in liver tissue Biomarker  Measure

 1) VLDL, ApoB, Cyp7α1

100 μl of serum and standard was separated into a 96 well plate and reacted at 37 ° C. for 90 minutes, and then washed three times using washing buffer. After washing, 100 μl of detection antibody was added and reacted again at 37 ° C. for 60 minutes and washed three times. Then, 100 μl of HRP-streptavidin cunjugate was added and reacted at 37 ° C. for 30 minutes, followed by washing. After reacting for 15 minutes at 50 μl and adding a 50 μl stop solution, the absorbance at 450 nm was measured using an ELISA reader, and the absolute value was expressed based on a standard curve.

2) StAR

100 μl of serum and standard was separated from the 96 well plate and 500 μl of the conjugate was added thereto, followed by reaction at 37 ° C. for 60 minutes. After the reaction was performed three times using the washing buffer. After washing, 50 μl of substrates A and B were added thereto, reacted for 15 minutes at 37 ° C., and 50 μl of stop solution was added to measure absorbance at 450 nm using an ELISA reader. Absolute values were expressed based on a standard curve.

3) LDL-receptor, Bile acyl-CoA synthetase

100 μl of serum and standard was added to the 96 well plate, and 100 μl of detection regent A was added thereto and reacted at 37 ° C. for 60 minutes. After the reaction was performed three times using the washing buffer. After washing, 100 μl of detection regent A was added and reacted at 37 ° C. for 60 minutes. After washing, 90 μl of substrate reagent was added and reacted at 37 ° C. for 15 minutes, and 50 μl of stop solution was added and absorbance at 450 nm through ELISA reader. Was measured and expressed as an absolute value based on the standard curve.

(7) Statistical Processing

The experimental results were statistically analyzed using unpaired student's T-test and ANOVA of SPSS 18.0 and tested for significance at p <0.001, p <0.01 and p <0.05.

Ⅱ. Experiment result

1. Liver Function

 1) AST

The results of AST were 150.9 ± 11.3 U / ℓ in the normal group, 231.9 ± 17.1 U / ℓ in the negative control group and 184.5 ± 28.6 U / L in the positive control group, while 193.8 ± 22.7 U / L in the MFC 200 and 400 administration groups. ℓ, 164.1 ± 9.3 U / ℓ, MFC administration group showed a significant (**: p <0.01, *: p <0.05) decrease compared to the negative control group (Fig. 1).

 2) ALT

As a result of measuring ALT, 41.1 ± 3.8 U / ℓ in the normal control group, 61.0 ± 7.8 U / ℓ in the negative control group and 48.0 ± 3.2 U / ℓ in the positive control group, while 52.0 ± 8.1 U / L in the MFC 200 and 400 administration group. ℓ, 47.7 ± 6.5 U / ℓ, MFC 400 administration group showed a significant (**: p <0.01) decrease compared to the negative control group (Fig. 2).

3) ALP

As a result of measuring ALP, 228.8 ± 48.2 U / l in normal group, 326.5 ± 43.0 U / l in negative control group and 258.7 ± 40.5 U / l in positive control group, 327.3 ± 51.5 U / l in MFC 200,400 group ℓ, 303.3 ± 59.1 U / ℓ, MFC 400-administered group was decreased compared to negative control group. No significance was shown (FIG. 3).

4) LDH

As a result of the LDH measurement, the normal control group showed 2148.4 ± 194.4 U / l, the negative control group showed 2284.8 ± 189.8 U / l, and the positive control group showed 2228.0 ± 260.3 U / l, whereas the MFC 200, 400 administration group showed 2220.7 ± 392.5 U / l. L, 2196.8 ± 380.0 U / L, showed no difference in all experimental groups (FIG. 4).

2. Impact on renal function

 1) BUN

As a result of measuring BUN, 12.5 ± 2.7 mg / dl for normal group, 16.5 ± 1.2 mg / dl for negative control group and 14.3 ± 1.7 mg / dl for positive control group, while 16.2 ± 2.5 mg / dl for MFC 200, 400 group ㎗, 16.7 ± 0.9 mg / 나타나, MFC administration group did not show a difference compared to the negative control group (Fig. 5).

 2) Creatinine

As a result of measuring creatine, 0.44 ± 0.06 ㎎ / dl for normal group, 0.45 ± 0.04 ㎎ / dl for negative control group and 0.45 ± 0.03 ㎎ / dl for positive control group, 0.41 ± 0.03 mg / dl for MFC 200, 400 group. ㎗, 0.40 ± 0.03 mg / dL, all experimental groups showed no difference (FIG. 6).

3. Lipid Metabolism Biomarkers in Blood

 TC (total cholesterol)

As a result of TC measurement, 510.8 ± 51.6 ng / ml for normal group, 1011.6 ± 122.6 ng / ml for negative control group and 753.9 ± 83.1 ng / ml for positive control group, 824.5 ± 87.7 ng / ml for MFC 200, 400 group. Ml, 773.4 ± 99.5 ng / ml, the MFC administration group showed a significant (**: p <0.01) decrease compared to the negative control group (FIG. 7).

 2) HDL-C (high density lipoprotein-cholesterol)

As a result of measuring HDL-C, 35.7 ± 17.1 ng / ml in normal group, 18.0 ± 11.7 ng / ml in negative control group and 72.5 ± 19.9 ng / ml in positive control group, while 73.8 ± 19.6 in MFC 200, 400 group. ng / ml, 119.0 ± 26.9 ng / ml, the MFC-administered group showed a significant (***: p <0.001, **: p <0.01) increase compared to the negative control group (FIG. 8).

3) LDL-C (low density lipoprotein-cholesterol)

As a result of measuring LDL-C, 327.8 ± 25.1 ng / ml in normal group, 831.3 ± 204.3 ng / ml in negative control group and 437.8 ± 115.1 ng / ml in positive control group, while 469.7 ± 120.5 in MFC 200, 400 group. ng / ml, 448.9 ± 168.1 ng / ml, the MFC-administered group showed a significant (**: p <0.01) decrease compared to the negative control group (FIG. 9).

4) TG ( triglycerides )

TG was measured to be 120.4 ± 28.3 ng / ml for the normal group, 509.5 ± 45.0 ng / ml for the negative control group and 411.8 ± 73.3 ng / ml for the positive control group, while 360.0 ± 96.5 ng / ml for the MFC 200 and 400 administration groups. Ml, 272.7 ± 28.7 ng / ㎖, MFC 400 administration group showed a significant (***: p <0.001) decrease compared to the negative control group (Fig. 10).

5) very low density lipoprotein (VLDL)

As a result of measuring VLDL, 190.5 ± 29.9 ng / ml in normal group, 334.9 ± 21.9 ng / ml in negative control group, 232.7 ± 42.5 ng / ml in positive control group, while 217.4 ± 20.5 ng / ml in MFC 200, 400 group. ㎖, 196.6 ± 15.2 ng / ㎖, MFC administration group showed a significant (***: p <0.001, **: p <0.01) decrease compared to the negative control group (Fig. 11).

6) arteriosclerosis index ( atherogenic  index)

Atherosclerotic index was measured as 3.9 ± 0.4 in normal group, 7.7 ± 0.9 in negative control group and 5.7 ± 0.6 in positive control group, while MFC 200 and 400 administration group showed 6.3 ± 0.7 and 5.9 ± 0.8, respectively. Administration group showed a significant (*: p <0.05) decrease compared to the negative control group (Fig. 12).

 7) cardiac risk factor

The cardiovascular risk index was found to be 5.9 ± 2.3 for the normal group, 15.6 ± 3.3 for the negative control group, and 7.6 ± 3.3 for the positive control group, while 9.8 ± 3.3 and 9.5 ± 3.7 for the MFC 200 and 400 groups, respectively. Was significantly (**: p <0.01, *: p <0.05) decrease compared to the negative control (Fig. 13).

4. Lipid metabolism in liver tissue Biomarker

 One) VLDL  (very low density lipoprotein)

As a result of measuring VLDL, it was 376.9 ± 80.2 pg / ml in normal group, 651.1 ± 130.9 pg / ml in negative control group and 411.0 ± 141.7 pg / ml in positive control group, while 325.9 ± 54.5 pg / ml in MFC 200 and 400 group. Ml, 368.8 ± 39.8 pg / ㎖, MFC administration group showed a significant (*: p <0.01, *: p <0.05) decrease compared to the negative control group (Fig. 14).

 2) ApoB (apolipoprotein B)

As a result of measuring ApoB, the normal control group showed 23.8 ± 5.0 ng / ml, the negative control group showed 66.6 ± 14.1 ng / ml, and the positive control group showed 55.0 ± 5.8 ng / ml, whereas the MFC 200, 400 administration group showed 66.9 ± 3.5 ng / ml. ㎖, 30.0 ± 5.1 ng / ㎖, MFC 400 administration group showed a significant (**: p <0.01, *: p <0.05) decrease compared to the negative control group (Fig. 15).

3) Cyp7α1  (cholesterol 7-α hydroxylase )

As a result of measuring Cyp7α1, the control group showed 13.6 ± 2.9 ng / ml, the negative control group showed 5.9 ± 0.8 ng / ml, and the positive control group showed 7.0 ± 2.3 ng / ml, whereas the MFC 200 and 400 administration groups were 5.3 ± 1.5 ng / ml. ㎖, 5.0 ± 1.4 ng / ㎖, MFC administration group showed a decrease compared to the negative control group (Fig. 16).

4) StAR (steroidogenic acute regulatory protein)

As a result of measuring StAR, 25.4 ± 4.7 ng / ml for the normal group, 16.2 ± 4.1 ng / ml for the negative control group and 19.4 ± 3.5 ng / ml for the positive control group, while 12.8 ± 3.0 ng / ml for the MFC 200 and 400 administration group. ㎖, 17.3 ± 2.0 ng / ㎖, MFC 400 administration group showed an increase compared to the negative control, but did not appear significant (Fig. 17).

5) LDL-receptor (low density lipoprotein-receptor)

As a result of measuring LDL-receptor, 30.8 ± 6.5 ng / ml in normal group, 16.7 ± 3.3 ng / ml in negative control group and 22.7 ± 7.7 ng / ml in positive control group, while 12.8 ± 3.0 in MFC 200 and 400 group. ng / ㎖, 9.3 ± 2.5 ng / ㎖, MFC administration group showed a decrease compared to the negative control group (Fig. 18).

6) Bile acyl - CoA synthetase

Bile acyl-CoA synthetase was measured as 745.0 ± 104.9 pg / ml for the normal group, 304.3 ± 56.2 pg / ml for the negative control group and 442.6 ± 62.7 pg / ml for the positive control group, while 226.6 for the MFC 200 and 400 administration groups. ± 32.5 pg / ㎖, 223.5 ± 18.5 pg / ㎖, MFC administration group showed a decrease compared to the negative control group (Fig. 19).

In order to objectively verify the efficacy of the antihyperlipidemic composition according to the present invention, various factors were identified through SD rats that induced hyperlipidemia with high cholesterol feed and 25% aqueous solution of fructose.

As a result of measuring liver function, AST and ALT were significantly decreased in the MFC group compared with the negative control group. ALP was decreased in the MFC 400 group compared with the negative control group, but there was no significant difference. LDH did not show any difference in all experimental groups.

As a result of measuring renal function, BUN and Creatinine did not show any difference in the MFC group compared to the negative control group.

In the blood lipid metabolism biomarkers, TC, LDL-C, VLDL, and TG were significantly decreased in the MFC-treated group compared to the negative control group, and HDL-C was significantly increased in the MFC-treated group compared to the negative control group. Appeared. Atherosclerotic index and cardiovascular risk index were also significantly decreased in MFC group compared with negative control group.

As a result of measuring lipid metabolism biomarkers in liver tissue, VLDL and ApoB were significantly decreased in MFC-treated group compared to negative control group, while StAR was increased in MFC 400-treated group compared with negative control group. . However, Cyp7α1, LDL-receptor, and Bile acyl-CoA synthetase were decreased in the MFC group compared with the negative control group.

Based on the above results, the antihyperlipidemic composition according to the present invention is a lipid diet such as cholesterol and triglycerides in the blood, as well as liver damage caused by hyperlipidemia in SD rats induced hyperlipidemia with cholesterol feed and 25% aqueous solution of fructose. Improvement efficacy for metabolic function has been experimentally identified.

However, VLDL and ApoB, which are related to LDL cholesterol, have been shown to decrease in liver tissue, which has been shown to be effective for hyperlipidemia. The efficacy on acyl-CoA synthetases was negligible or absent.

Therefore, in-depth studies using blood and tissues may provide a basis for treating hyperlipidemia if the results of clinical studies are supported with the enhancement of other biomarker efficacy related to hyperlipidemia.

The present invention provides a composition having an antihyperlipidemic effect consisting of the above-described configuration and function.

The present invention is very useful in the business of producing, manufacturing, selling, distributing, and researching antihyperlipidemic efficacy and therapeutic compositions.

Claims (3)

Natural composition with antihyperlipidemic effect, which is a mixture of persimmon soup, licorice, missing name, Angelica, Sansa, Saenghwanghwang, Shiho, Injinho, Chajeon, Sewao and Red Ginseng,
A composition having an antihyperlipidemic effect, which is prepared by mixing fermented antler extract.
The method of claim 1,
The natural composition is 80 to 120 parts by weight of licorice, 80 to 120 parts by weight, Angelica 80 to 120 parts by weight, hawthorn 80 to 120 parts by weight, 80 to 120 parts by weight of raw sulfur, 80 to 120 parts by weight Part, Injin-Ho 80-120 parts by weight, 80-120 parts by weight of chajeon, 80-120 parts by weight of sewage, 80-120 parts by weight of red ginseng extract composition characterized in that the antihyperlipidemic effect.
A pharmaceutical composition efficacious in preventing and treating hyperlipidemia, comprising the composition having an antihyperlipidemic effect of claim 1.

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