KR100877604B1 - Composition comprising an extract of processed ginseng for preventing and treating obesity - Google Patents

Abstract

The present invention relates to a composition for the prevention and treatment of obesity containing a processed extract of Panax plants with enhanced potency, ginsenosides (Rg3 + Rg5 + Rk1) / (Rb1 + Rb2 + Rc + Ginseng extract obtained by special processing treatment with a ratio of Rd) of 1.0 or more reduced weight of obese rats increased due to estrogen deficiency due to ovarian extraction, and blood cholesterol, low density lipoprotein (LDL) and triglyceride concentrations. At the same time reduce the concentration of high-density lipoprotein (HDL) in the blood, and inhibits the fat accumulation of the nematode ( C. elegan) can be useful as a composition for the prevention and treatment of obesity.

Panax genus, Ginseng, Obesity, Estrogen, Total cholesterol, Neutral lipid, HDL, LDL, Pharmaceutical composition, Health food.

Description

Composition comprising an extract of processed ginseng for preventing and treating obesity

1 is a diagram showing the change in weight of rats for each experimental group following SG 6-week administration,

Figure 2 is a diagram showing the total cholesterol content in the serum of each experimental group according to SG administration,

3 is a diagram showing the content of neutral lipids in the serum of each experimental group according to SG administration,

Figure 4 is a diagram showing the HDL content of serum of each experimental group according to SG administration,

5 is a diagram showing the LDL content of serum of each experimental group according to SG administration,

Figure 6 is a diagram showing whether the inhibition of the production of lipid granules (Lipid Droplet) in the little nematode ( C. elegans ) following SG administration.

The present invention relates to a composition for the prevention and treatment of obesity, containing the processed extract of the genus Panax plant as an active ingredient.

Obesity is the most common nutritional problem in the industrial community, according to US statistics, one third of the American population and 20% of children are reported as obese, and over 70% of people with type 2 diabetes are obese. There is an increased risk of developing hypertension, hyperlipidemia and some cancers. It is well known that carbohydrate metabolism abnormalities and insulin-independent diabetes mellitus are often associated with obese people, and that weight gain exacerbates existing diabetes conditions, but the exact nature of the relationship between obesity and diabetes is still controversial. . Since not all people with severe obesity have diabetes, it is believed that obesity itself is not sufficient to cause insulin non-dependent diabetes and diabetes is caused by a combination of genetic predisposition or environmental factors for diabetes. However, the incidence of insulin-independent diabetes is much higher in obese people, and since the incidence of insulin-independent diabetes is closely related to past obesity and duration, obesity is a powerful risk factor for insulin-independent diabetes.

On the other hand, not only the degree of obesity but also the distribution of fat is known to be closely related to the disease risk associated with obesity, abdominal fat is particularly problematic.

Insulin-dependent diabetes patients often have a history of obesity or obesity. In the case of Westerners, 60-90% of the non-insulin-dependent diabetics are obese, and about 70% of the non-insulin-dependent diabetes patients in Korea have a history of obesity (Park Joong-yeol et al. Weight change patterns, diabetes, 17 , pp. 51-57, 1993).

Many prospective studies have also shown that obesity precedes glucose tolerance and insulin-independent diabetes (Carey VJ. Et al., Body fat distribution and risk of non-insulin-dependent diabetes mellitus in women, The nurses' health study, Am J Epidemiol , 145 , pp. 614-619, 1997). In the Framingham study, obesity was found to be more common in obese people, and in most studies, obese people with impaired glucose tolerance were at higher risk for developing insulin-independent diabetes.

The exact mechanism of progression from obesity to diabetes is unknown, but increased insulin resistance is believed to play an important role. Felber et al. Reported that obesity is associated with normal glucose tolerance, impaired glucose tolerance, diabetes with hyperinsulinemia and diabetes with hypoinsulinemia, according to epidemiological observations. It was classified into four groups and progressed from obesity to diabetes (Golay A. et al., Obesity and NIDDMP, the retrograde regulation concept, Diabetes Rev , 5 , pp.69-82, 1997).

In obesity, carbohydrate metabolism is normal in blood glucose response to cervical glucose load but insulin resistance is higher than normal. Insulin resistance is more than one of the main pathophysiology of obesity and obese insulin non-dependent diabetics. Observed from the beginning. Various hypotheses have been suggested as to what mechanisms reduce insulin action in obesity, but it is not yet clear. In other words, the decrease in function of insulin receptors, glucose transporters, enzymes involved in glycogen synthesis and glucose oxidation are observed during obesity, but is understood as a secondary phenomenon due to obesity (Golay A. et al., Obesity and NIDDMP, the retrograde regulation concept, Diabetes Rev , 5 , pp. 69-82, 1997).

Given the contextual evidence, it is thought that adipocytes contribute to the development of insulin resistance, that is, factors or metabolic messengers secreted from adipocytes are expected to inhibit the action of insulin in muscle and liver. The first and most widely recognized of these factors is the free fatty acids that are hydrolyzed from triglycerides stored in adipose tissue. In addition, TNF- and leptin released from adipocytes have recently been suggested as a cause of insulin resistance in obesity (Hotamisligil GS. Et al., Tumor necrosis factor a, a key component of the obesity-diabetes link, Diabetes , 43 , pp. 1271-1278, 1994; Cohen B., Novick D., Rubinstein M., Modulation of insulin activities by leptin, Science , 274 , pp. 1185-1188, 1996).

In obesity, energy metabolism is mainly lipid, and both lipid breakdown and lipid synthesis are increased. Increased lipolysis and thus increased use of free fatty acids are a hallmark of obesity, especially abdominal obesity, and a high correlation between fat volume and lipid oxidation is observed, suggesting that increased fat volume may contribute to increased free fatty acid levels and lipid oxidation. I think. Lipid oxidation is observed in the early stages of obesity, and is also increased on fasting or after sugar loading.

In recent years, as the eating habits have been westernized and the culture level has been improved, simple obesity has increased significantly. Obesity has been a cause of involvement or exacerbation of various diseases such as hypertension, arteriosclerosis, fatty liver and diabetes. Therefore, it is better to prevent obesity in advance, and if obesity is to control the body metabolism smoothly through the reduction of body fat and lipid metabolism is very important for the prevention and health of various diseases.

In particular, the incidence of obesity is increasing in menopausal women, which is known to be the primary cause of estrogen deficiency due to ovarian dysfunction (Kim Sang-man, postmenopausal obesity . Journal of the Korean Society of Obesity, 10 (3) , pp217-226, 2001) .

Estrogens inhibit fat accumulation by inhibiting the action of lipoprotein lipase (LPL) in adipocytes (Hamosh M. et al., J Clin Invest ., 55 , pp11321135, 1975). Deficiency of estrogens increases the action of lipoproteinlipase, resulting in fat accumulation and fat gain in adipocytes, which can be inhibited by estradiol (E2) administration (Geary, N. et al., J.) . Physiol. Regul. Intergr. Comp. Physiol., 281, pp1290-1294, 2001). This action of estradiol (E2) induces hormone sensitive lipase (Palin SL et al., Metabolism , 52 , pp383388, 2003) or increases fatty acid β oxidation of epinephrine (lipin accumulation). Appears to be inhibited (Ackerman GE et al., Endocrinology , 109 , pp20842088, 1981). In addition, it exhibits a suppression of adipocyte production from bone marrow stromal cells (Heim M. et al., Endocrinology , 145 , pp848859, 2004; Okazaki, R. et al., Endocrinology , 143 , pp2349- 2356, 2002; Homma, H. et al., J. Biol . Chem ., 275 , pp5793-5796, 2000), increase cholesterol metabolism and promote cholesterol absorption and degradation (Hewitt KN, et al., Endocrinology , 145 , pp18421848, 2004).

Meanwhile, lipid metabolism abnormalities and atherosclerosis and circulatory diseases caused by estrogen deficiency have been increased (Mendelsohn, ME et al., Circ . Res . , 87 , pp956-960, 2000; Mendelsohn, ME et al., N. Engl . J. Med . , 340 , pp 1801-1811, 1999). This suggests that estrogens may be expressed in IL-1 induced vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule (E-selectin) and intercellular adhesion molecule-1, in vascular endothelial cells. ICAM-1) (Caulin-Glaser, T. et al., J. Clin . Invest , 98 , pp36-42, 1996) to inhibit the interaction of monocytes and vascular endothelial cells. Consistent with the report (Nathan, L. et al., Circ ., 85 , pp377385, 1999). In addition, estrogen lowers blood cholesterol and LDL (Hough, JL et al., Arteriosclerosis , 6 , pp5763, 1986) and reacts with HDL to esterify cholesterol (Banka, CL et al., Harwood Academic Publishers, Amsterdam , pp91106, 1998; Abplanalp, W. et al., J. Endocrinol . , 142 , pp7983, 2000). In addition, oxLDL production of macrophages can be suppressed (Sack, MN et al., Lancet . , 343 , pp269270, 1994) and macrophage can inhibit circulatory disease by inhibiting the expression of vascular wall thickening factor (Shanker, G., et al., Lymphokine Cytokine Res ., 13 , pp 1-7, 1994; Shanker, G. et al., Life Sci ., 56 , pp 499507, 1995).

As described above, obesity, which is indicated by estrogen deficiency in menopausal women, may cause hyperlipidemia and arteriosclerosis due to abnormal lipid metabolism, and may cause cardiovascular diseases and various metabolic diseases. Therefore, in order to prevent and treat such diseases, weight loss and inhibiting fat cell function may be very important.

Ginseng is a perennial plant belonging to the genus Panax, and the genus Panax is a perennial root of the genus Araliaceae. Consider a typical species of ginseng (Panax ginseng), hwagisam (Panax quinquefolia ), Whole Chilsam (samchi, Panax notoginseng ), bamboo ginseng ( Panax japonica ), trilobite ( Panax trifolia ), Himalayan ginseng ( Panax pseudoginseng ) and Panax vietnamensis (Understanding Korean Ginseng, Korean Ginseng Society, p9, 1995; Advances in Ginseng Research, Korean Ginseng Society, pp 127-137, 1998). Other Panax plants include Panax elegathior ( Panax elegatior ), Panax wanzianus ( Panax wangianus), Panax non pinra typhus (Panax bipinratifidus ).

The most important component in these Panax plants is saponin. In particular, the genus Panax plants, unlike other plants, contain a common saponin with 1-4 sugars bound to the dammarane skeleton. In particular, saponins with high content in Korean ginseng are ginsenosides Rb1, Rb2, Rc, Rd, Rg1 and Re. These saponin components have various effects, and the types and strengths of the drugs vary greatly depending on their structure (Understanding Korean Ginseng, Korean Ginseng Society, p9, 1995).

Ginseng has long been known to be effective for fatigue recovery and strength enhancement. In fact, ginseng is known to have increased exploratory activity, decreased spontaneous movement, elevated seizure threshold, increased memory and analgesic effects (Understanding Korean Ginseng, Korean Ginseng Society, p9, 1995). In addition to these effects, it has been applied to improvement of anxiety neurosis, insomnia, depression, and postpartum psychiatric symptoms (herbal medicine, Hakchangsa, 2003).

However, the ginseng's effect is very weak.

Recently, there have been attempts to enhance the efficacy of ginseng by applying various processing methods to ginseng. The most representative method is the method developed by Park et al. Park et al. Developed a method of specially processing ginseng under high temperature and high pressure conditions (Korean Patent No. 192678, US Patent No. 5776460). In this process, ginsenosides Rb1, Rb2, Rc, and Rd, which are mainly contained in ginseng, are changed to ginsenosides Rg3, Rg5, and Rk1, which are not present in ginseng, and various new medicinal ingredients are produced to prevent antioxidant activity. , Anticancer activity, blood circulation improvement, etc. are very enhanced (Kim WY et al., J. Nat . Prod . , 63 (12), pp1702-1704; Kwon SW et al., J. Chromatogr A. , 921 ( 2), pp 335-339, 2001). In particular, Rg3, Rg5, and Rk1 are known to have strong potency, and as shown in FIG. 1, some of the sugars in gallenolan glycosides such as ginsenosides Rb1, Rb2, Rc and Rd originally present in ginseng during processing It either comes off or continues to dehydrate at the 20th carbon position. Therefore, these components are produced by processing any plant containing glycoside glycosides. Korean ginseng ( Panax ginseng ), American hemp ( Panax quinquefolia ), Whole Chisam (Samchi, Panax) notoginseng ), Panax japonica , Trilobite ( Panax) trifolia ), Himalayan ginseng ( Panax pseudoginseng ), Vietnamese ginseng ( Panax vietnamensis ), Panax elegathior ( Panax elegatior ), Panax wanzianus ( Panax wangianus ) , or Panax bifinatipidus ( Panax Roots, stems, or leaves of bipinratifidus ) contain glycosides in common, so Rg3, Rg5, and Rk1 extracts have been enhanced using the method of Park et al. (Korean Patent No. 192678, US Patent No. 5776460). Can be obtained. However, to date, there has been no disclosure or study on the efficacy of these ingredients and ginseng specially processed by the above method for obesity.

The present inventors specially processed ginseng extract ginsenosides Rg3, Rg5 and Rk1 the sum of the content of ginsenosides Rb1, Rb2, Rc and Rd of the special processed ginseng extract and Rg3, Rg5 and The present invention was completed by confirming that the fraction containing Rk1 has an excellent inhibitory effect on obesity.

An object of the present invention is a specially processed Panax genus plants extracts of the processed Panax genus plants increased the active ingredient so that the ratio of ginsenosides (Rg3 + Rg5 + Rk1) / (Rb1 + Rb2 + Rc + Rd) is 1.0 or more It provides a composition for the prevention and treatment of obesity containing as an active ingredient.

In order to achieve the above object, the present invention is effective for extracts of the processed Panax genus plants with increased active ingredient so that the ratio of ginsenoside (Rg3 + Rg5 + Rk1) / (Rb1 + Rb2 + Rc + Rd) is 1.0 or more It provides a pharmaceutical composition for the prevention and treatment of obesity containing as an ingredient.

Rg3 as defined herein includes two isomers, (20-S) and (20-R).

The present invention provides a pharmaceutical composition for the prevention and treatment of obesity, containing ginseng processed extract prepared by heating the Panax genus plant extract for 2 to 6 hours at a high temperature of 70 to 150 ℃.

In addition, the Panax genus plants defined herein include Panax ginseng , Panax quinquefolia , Panax ginseng , Panax notoginseng , Panax japonica , Panax ginseng, Panax trifolia), Himalayan cedar (outpost, the roots of Panax pseudoginseng), Vietnam, three (Panax vietnamensis), Panax elegans tee climb (Panax elegatior), Panax Wan Jia Augustine (Panax wangianus) or Panax non pinra Tippi Douce (Panax bipinratifidus), Plants such as stems or leaves.

The extract means an extract soluble in water, lower alcohols of C ₁ to C ₄ and mixed solvents thereof, preferably ethanol.

Hereinafter, the present invention will be described in detail.

Processed ginseng extract of the present invention, the dried Panax genus plants are chopped into the autoclave sterilizer at 70 ℃ to 150 ℃, preferably 100 ℃ to 130 ℃ about 2 hours to 6 hours, preferably 3 hours to 5 hours After heating for about 1 to 20 times the weight (kg), preferably about 3 to 10 times water, C ₁ to C ₄ lower alcohol or a mixed solvent thereof, preferably ethanol, The extract obtained by using a reflux extraction method for about 3 hours to 10 hours, preferably about 3 hours to 6 hours, was filtered, concentrated under reduced pressure or dried, and then the obtained extract was heated to 40 ° C to 80 ° C, preferably 50 ° C. The dried ginseng extract of the present invention may be obtained by drying at 70 ° C. to 70 ° C.

In order to confirm the anti-obesity effect of the extract, experiments on estrogen deficiency obesity induction and drug administration and experiments on fat accumulation of C. elegans , the extract of the present invention prevents and treats obesity It could be confirmed that indicates.

Since the extract of the present invention has little toxicity and side effects, it can be used safely even when taken for a long time for the purpose of prevention.

The present invention provides a pharmaceutical composition for the prevention and treatment of obesity containing the processed ginseng extract obtained by the above method as an active ingredient.

The pharmaceutical composition of the present invention preferably contains 0.01 to 99% of the extract, more preferably 0.02 to 50%. The above content does not limit the scope of the present invention in any aspect.

Accordingly, the present invention provides a pharmaceutical composition for the prevention and treatment of obesity, including the extract obtained by the above method as an active ingredient, and containing a pharmaceutically acceptable carrier or excipient.

Pharmaceutical compositions comprising the extract of the present invention may further comprise suitable carriers, excipients and diluents commonly used in the manufacture of pharmaceutical compositions.

Pharmaceutical compositions comprising the extract of the present invention, respectively, in the form of powders, granules, tablets, capsules, suspensions, emulsions, syrups, aerosols, oral formulations, external preparations, suppositories, and sterile injectable solutions according to conventional methods. Can be used. Carriers, excipients and diluents which may be included in the composition comprising the extract of the present invention include lactose, dextrose, sucrose, sorbitol, mannitol, xylitol, erythritol, maltitol, starch, acacia rubber, alginate, gelatin, calcium phosphate , Calcium silicate, cellulose, methyl cellulose, microcrystalline cellulose, polyvinyl pyrrolidone, water, methylhydroxybenzoate, propylhydroxybenzoate, talc, magnesium stearate and mineral oil. When formulated, diluents or excipients such as fillers, extenders, binders, wetting agents, disintegrating agents, and surfactants are usually used. Solid form preparations for oral administration include tablets, pills, powders, granules, capsules, and the like, and the solid form may include at least one excipient such as starch, calcium carbonate, sucrose in the extract. ) Or lactose, gelatin and the like are mixed. In addition to simple excipients, lubricants such as magnesium stearate and talc are also used. Oral liquid preparations include suspensions, solvents, emulsions, and syrups, and may include various excipients, such as wetting agents, sweeteners, fragrances, and preservatives, in addition to commonly used simple diluents such as water and liquid paraffin. . Formulations for parenteral administration include sterile aqueous solutions, non-aqueous solvents, suspensions, emulsions, lyophilized preparations, suppositories. As the non-aqueous solvent and suspending agent, propylene glycol, polyethylene glycol, vegetable oil such as olive oil, injectable ester such as ethyl oleate and the like can be used. As the base of the suppository, witepsol, macrogol, tween 61, cacao butter, laurin butter, glycerogelatin and the like can be used.

Preferred dosages of the extracts of the present invention vary depending on the condition and weight of the patient, the extent of the disease, the form of the drug, the route of administration and the duration, and may be appropriately selected by those skilled in the art. However, for the desired effect, the extract of the present invention is preferably administered at 0.0001 to 100 mg / kg, preferably 0.001 to 100 mg / kg per day. Administration may be administered once a day or may be divided several times. The dosage does not limit the scope of the invention in any aspect.

The extract of the present invention can be administered to mammals such as mice, mice, livestock, humans, etc. by various routes. All modes of administration can be expected, for example, by oral, rectal or intravenous, intramuscular, subcutaneous, intrauterine dural or intracerebroventricular injection.

The present invention is for the prevention and improvement of obesity containing the extract of the processed Panax genus plants with increased active ingredient so that the ratio of ginsenoside (Rg3 + Rg5 + Rk1) / (Rb1 + Rb2 + Rc + Rd) is 1.0 or more Provide dietary supplements.

In addition, the present invention provides a health functional food for the prevention and improvement of obesity containing ginseng processed extract prepared by heating the Panax genus plant extract for 2 to 6 hours at a high temperature of 70 to 150 ℃.

Examples of the food to which the extract of the present invention can be added include various foods, beverages, gums, teas, vitamin complexes, and health functional foods.

 The extract of the present invention may be added to food or beverages for the purpose of preventing and improving obesity. At this time, the amount of the extract in the food or beverage may be added in 0.01 to 15% by weight of the total food weight, the health beverage composition may be added in a ratio of 0.02 to 5 g, preferably 0.3 to 1 g based on 100 ml. have.

The health functional beverage composition of the present invention is not particularly limited to other ingredients except for having the extract as an essential ingredient in the indicated ratio, and may contain various flavors or natural carbohydrates, etc. as additional ingredients, as in general beverages. Examples of the above-mentioned natural carbohydrates include monosaccharides such as glucose, fructose and the like; Disaccharides such as maltose, sucrose and the like; And conventional sugars such as polysaccharides such as dextrin, cyclodextrin, and sugar alcohols such as xylitol, sorbitol, and erythritol. As flavoring agents other than those described above, natural flavoring agents (tauumatin, stevia extract (e.g., Rebaudioside A, glycyrrhizin, etc.) and synthetic flavoring agents (saccharin, aspartame, etc.) can be advantageously used. The proportion of said natural carbohydrates is generally about 1-20 g, preferably about 5-12 g per 100 ml of the composition of the present invention.

In addition to the above, the extract of the present invention includes various nutrients, vitamins, minerals (electrolytes), flavors such as synthetic flavors and natural flavors, coloring and neutralizing agents (such as cheese and chocolate), pectic acid and salts thereof, alginic acid and its Salts, organic acids, protective colloidal thickeners, pH adjusting agents, stabilizers, preservatives, glycerin, alcohols, carbonation agents used in carbonated drinks, and the like. In addition, the extract of the present invention may contain natural fruit juice and fruit flesh for the production of fruit juice beverages and vegetable beverages. These components can be used independently or in combination. The proportion of such additives is not so critical but is usually selected in the range of 0 to about 20 parts by weight per 100 parts by weight of the extract of the present invention.

Below, The invention is illustrated in detail by the following examples and experimental examples.

However, the following Examples and Experimental Examples are only illustrative of the present invention, the contents of the present invention is not limited by the following Examples, Reference Examples and Experimental Examples.

Reference Example 1. Preparation of Laboratory Animals

Experimental animals were supplied with 5 week-old female S.D (Sprague-Dawley) rats (weight 190-210 g) from Daehan Biolink and used for 1 week in the laboratory. The kennel controlled the lighting time by artificial lighting equipment from 7:00 am to 7:00 pm for 12 hours, and kept the room temperature around 22 ℃ and the humidity around 60%. The feed was fed a solid feed (Samyangsa, Korea) consisting of 21% protein, 3.5% fat, 5.0% cellulose and 8.0% minerals. .

Reference Example 2. Statistics Processing

The significance test for the following experimental results was performed using the student's t-test.

Example  1. Preparation of Processed Ginseng Extract

The processed ginseng extract used in the present invention was supplied by Ginseng Science Co., Ltd., and processed ginseng extract prepared by the method of preparing Korean Patent Application No. 10-2005-0086650 (composition for preventing and treating diseases caused by vascular damage). It was used as, the manufacturing method is as follows.

Kim et al. (Kim WY et al., J. Nat. Prod. , 63 (12) , pp1702-1704; Kwon SW et al., J. Chromatogr A. , 921 (2) , pp335-339, 2001) Processed ginseng was prepared by. 1 kg of dried processed ginseng was put into an autoclave and heated using steam at 120 ° C. for 4 hours. 2 L of ethanol was added to the heated ginseng, refluxed for 4 hours in a water bath, filtered, and the solvent was evaporated to dryness to prepare 300 g of the ginseng extract of the present invention (hereinafter, referred to as SG).

Example 2 Ginsenoside Content Analysis of Processed Ginseng

The processed ginseng, unprocessed white ginseng, and red ginseng saponins prepared according to the present invention were analyzed by the following method.

The processed ginseng prepared in Example 1 was pulverized into powder using a grinder, 1 g of each was taken into a 50 mL flask, and refluxed three times with 20 mL of 70% ethanol for 3 hours to collect the extract. Each extract was concentrated by evaporation under reduced pressure, and the remaining residue was dissolved in methanol to make 20 mL, which was used as a processed ginseng sample solution.

Separately, white ginseng and red ginseng purchased on the market were extracted in the same manner to prepare white and red ginseng samples.

As a result of analyzing each saponin component by HPLC according to the method of the literature (Vol. Et al., Journal of Chromatography A , Vol. 921, pp 335-339), using the ginsenoside Rb1 and Rg3 standard solutions as shown in Table 1 below.

As shown in Table 1, in the case of processed ginseng at the ginsenoside relative peak area, the sum of (Rg3 + Rg5 + Rk1) is higher than the sum of (Rb1 + Rb2 + Rc + Rd).

Rb1 Rb2 Rc Rd Rg3 Rg5 Rk1 (Rg3 + Rg5 + Rk1) / (Rb1 + Rb2 + Rc + Rd) Processed ginseng 1.46 3.91 3.11 0.59 34.2 8.94 12.5 6.1 White ginseng 18.5 12.1 14.3 6.66 0 0 0 0 Red ginseng 16.3 9.05 11.4 5.34 1.05 0.55 0.34 0.046

Experimental Example  1. Estrogen deficiency Obesity induction  And drug administration experiments

Rats were injected intramuscularly by intramuscular injection of ketamine at 1 ml / kg and the abdominal hairs were removed. After disinfection of the surgical site with 70% ethanol (EtOH), the skin, abs and peritoneum were dissected to about 1 cm and the ovaries were exposed, followed by excision and suture. The normal group underwent sham resection only to the peritoneal incision of the rat, and then re-sealed without ovarian extraction.

The experiment was divided into four groups. That is, 200 mg of the SG obtained in Example 1 after the peritoneal incision, mock surgery normal group (NC) without ovarian extraction, ovarian extraction operation, experimental control group without drug (OC), and ovarian extraction operation / kg orally administered group (SGH) and after ovarian extraction, the SG obtained in Example 1 was divided into 100mg / kg orally administered group (SGL). The animals used for the experiment were 10 animals for the mock surgery group and the control group, and 8 animals for the large and small dose administration groups. After the drug was dissolved in physiological saline, lyophilized SG was administered once a day for 6 weeks.

After 24 hours of drug administration, blood was collected and centrifuged at 3,000 rpm for 10 minutes to obtain 20 μl of the upper layer, followed by total cholesterol (TC), high density lipoprotein (HDL) and triglyceride (TG). The content was measured using a kit (Youngdong Pharmaceutical).

Low density lipoprotein (LDL) content was calculated by Friedewald formula (1).

Low Density Lipoprotein (LDL)

= Total cholesterol-High density lipoprotein (HDL)-1/5 Triglyceride

1-1. Weight change

 As shown in Table 2 and FIG. 1, the body weight was measured 6 weeks after drug administration, and the normal group was about 224.4 g, and the control group was 276.8 g, the high dose SG group (SGH), 263.1 g and the low dose SG group (SGL). Measured at 259.3 g.

The control group showed a significant increase in body weight compared to the normal group, and the experimental group high-dose group (SGH) and low-dose group (SGL) decreased in weight compared to the control group.

Changes in the weight of rats in each experimental group following SG administration (g) NC OC SGH SGL Week 1 195.3 196.4 203.7 200.5 2nd week 202.8 220.3 215.3 219.2 3 weeks 208.1 243.2 231.3 236.2 4 weeks 215.4 260.9 235.2 243.2 Week 5 215.4 265.3 250.4 252.1 Week 6 224.4 276.8 263.1 259.3

1-2. Total Cholesterol Content

As shown in Table 3 and Figure 2, the total cholesterol content in serum was 52.7 ± 14.5 mg / dl in the normal group, significantly increased to 79.4 ± 11.4 mg / dl in the control group than the normal group.

In the experimental group, the high dose group (SGH) decreased to 66.1 ± 8.1 mg / dl compared to the control group, and the low dose group (SGL) decreased to 71.6 ± 6.4 mg / dl compared to the control group.

Total Cholesterol Content in Serum of Rats Subjected to SG Administration Experiment group Total cholesterol (mg / dl) NC    52.7 ± 14.5 * OC  79.4 ± 11.4 SGH 66.1 ± 8.1 SGL  71.6 ± 6.4 A) Mean ± Standard Error *: Statistically clear difference from the estrogen-deficient control. (*: p <0.05 vs OC)

1-3. Neutral lipid content

As shown in Table 4 and Figure 3, the triglyceride content in serum was 69.2 ± 7.5 mg / dl in the normal group, significantly increased to 111.2 ± 34.2 mg / dl in the control group compared to the normal group.

In the experimental group, the high dose group (SGH) was significantly reduced to 97.6 ± 16.3 mg / dl.

Neutral Lipid Contents in Serum of Rats Following SG Administration Experiment group Triglyceride (mg / dl) NC   69.2 ± 7.5 * OC 111.2 ± 34.2 SGH  97.6 ± 16.3 * SGL  128.5 ± 30.0 A) Mean ± Standard Error *: Statistically clear difference with the estrogen-deficient control. (*: p <0.05 vs OC)

1-4. HDL-cholesterol content

As shown in Table 5 and Figure 4, the HDL-Cholesterol content in the serum was 46.58 ± 8.22 mg / dl in the normal group, 37.75 ± 5.44 mg / dl in the control group significantly reduced compared to the normal group.

In the experimental group, the high dose group (SGH) was 46.15 ± 6.06 mg / dl compared to the control group, and the low dose group (SGL) was 35.80 ± 5.67 mg / dl compared to the control group.

Serum HDL Cholesterol Content in Rats Following SG Administration Experiment group HDL-Cholesterol (mg / dl) NC 46.58 ± 8.22 * OC 37.75 ± 5.44 SGH 46.15 ± 6.06 * SGL 35.80 ± 5.67 A) Mean ± Standard Error *: Statistically clear difference from the estrogen-deficient control. (*: p <0.05 vs OC)

1-5. LDL Cholesterol content

As shown in Table 6 and FIG. 5, the serum LDL-Cholesterol content was 17.8 ± 7.02 mg / dl in the normal group, and significantly increased compared to the normal group in 17.8 ± 7.02 mg / dl in the control group.

In the experimental group, the high dose group (SGH) was significantly reduced to 16.5 ± 10.74 mg / dl compared to the control group, and the low dose group (SGL) was significantly reduced to 19.1 ± 16.50 mg / dl compared to the control group.

LDL Cholesterol Content in Serum of Rats Subjected to SG Administration Experiment group LDL-Cholesterol (mg / dl) NC 17.8 ± 7.02 ** OC 17.8 ± 7.02 SGH 16.5 ± 10.74 ** SGL 19.1 ± 16.50 ** A) Mean ± Standard Error *: Statistically clear difference from the estrogen-deficient control. (*: p <0.05 vs OC)

Experimental Example  2. Little eelworm( C. elegans )of  Experiment on fat accumulation

In order to determine whether the SG obtained in Example 1 by SG nematode ( C. elegans ) inhibits the production of Lipid Droplet (Lipid Droplet) by applying the method described in the existing literature by the following process Nile Red (Nile Red) staining was performed (Greenspan P. et al., J Cell Biol ., 100 (3) , pp 965-73, 1985). Nile red (Nile Red) is a dyeing material that can confirm the degree of accumulation of fat granules by dyeing fat granules with oil red (Oil Red).

One small nematode of the L4 stage was transferred per plate and divided into a control group and a treatment group, and the treated group was treated with 10 g / ml of SG, respectively. The next day, the P0 generation was removed and the plate was treated with Nile red solution, followed by incubation for 3 days. The small nematodes of each plate were fixed with sodium azide (NaN ₃ ), and then photographed by observing at RFP length (628 nm) × 400 using a fluorescence microscope.

SGs were treated with small nematodes at a concentration of 10 μg / ml, and the lipid granules (Lipid Droplet) were subjected to nile red staining and measured by optical and fluorescence microscopy. A, C are optical microscopy, B, D is a group measured by fluorescence microscope fat granules.

As a result, as shown in Figure 6, A, B is a control group, C, D was found to reduce fat in the SG treatment group.

Hereinafter, the preparation examples of the pharmaceutical composition and health functional food will be described, but the present invention is not intended to be limited thereto, but is intended to be described in detail.

Formulation example  One. Powder  Produce

20 mg of SG of Example 1

Lactose 100 mg

Talc 10 mg

The above ingredients are mixed and filled in an airtight cloth to prepare a powder.

Formulation example  2. Preparation of Tablets

SG 10 mg of Example 1

Corn starch 100 mg

Lactose 100 mg

2 mg magnesium stearate

After mixing the above components, tablets are prepared by tableting according to a conventional method for preparing tablets.

Formulation example  3. Manufacture of capsule

SG 10 mg of Example 1

3 mg of crystalline cellulose

Lactose 14.8 mg

Magnesium Stearate 0.2 mg

According to a conventional capsule preparation method, the above ingredients are mixed and filled into gelatin capsules to prepare capsules.

Formulation example  4. Preparation of Injectables

SG 10 mg of Example 1

Mannitol 180 mg

Sterile distilled water for injection 2974 mg

Na ₂ HPO ₄ , 12H ₂ O 26 mg

According to the conventional method for preparing an injection, the amount of the above ingredient is prepared per ampoule (2 ml).

Formulation example  5. Liquid  Produce

20 mg of SG of Example 1

10 g of isomerized sugar

5 g of mannitol

Purified water

According to the conventional method of preparing a liquid solution, each component is added and dissolved in purified water, lemon flavor is added thereto, the above components are mixed, and then, purified water is added to adjust the total volume to 100 ml, and then sterilized by filling into a brown bottle. do.

Formulation example  6. Manufacture of healthy food

SG 1000 mg of Example 1

Vitamin mixture proper amount

70 μg of Vitamin A Acetate

Vitamin E 1.0 mg

Vitamin B ₁ 0.13 mg

Vitamin B ₂ 0.15 mg

Vitamin B ₆ 0.5 mg

0.2 μg of vitamin B ₁₂

Vitamin C 10 mg

10 μg biotin

Nicotinic Acid 1.7 mg

50 μg folic acid

Calcium Pantothenate 0.5mg

Mineral mixture

Ferrous Sulfate 1.75 mg

Zinc Oxide 0.82 mg

Magnesium carbonate 25.3 mg

Potassium monophosphate 15 mg

Dibasic calcium phosphate 55 mg

100 mg potassium citrate

Magnesium chloride 24.8 mg

Although the composition ratio of the above-mentioned vitamin and mineral mixtures is mixed with a component suitable for a health food in a preferred embodiment, the compounding ratio may be arbitrarily modified, and the above ingredients are mixed according to a conventional health food manufacturing method. The granules may be prepared and used for preparing a health food composition according to a conventional method.

Formulation example  7. Manufacture of health drinks

SG 1000 mg of Example 1

Citric acid 1000 mg

100 g oligosaccharides

Plum concentrate 2 g

1 g of taurine

Add 900 ml of purified water

After mixing the above components according to the conventional healthy beverage production method, and then stirred and heated at 85 ℃ for about 1 hour, the resulting solution is filtered and obtained in a sterilized 2 L container, sealed sterilization and then refrigerated and stored Used to prepare the healthy beverage composition of the invention.

The processed ginseng extract of the present invention reduces the weight of obese rats increased due to estrogen deficiency due to ovarian extraction, and decreases blood cholesterol, low density lipoprotein (LDL) and triglyceride concentrations, and high density lipoprotein (HDL) concentration in blood. Increasing and inhibiting the fat accumulation of C. elegan can be useful as a composition for the prevention and treatment of obesity.

Claims (7)

Contains processed extracts of Panax ginseng or Panax quinquefolia from which ginsenosides (Rg3 + Rg5 + Rk1) / (Rb1 + Rb2 + Rc + Rd) have been increased to an active ingredient of 1.0 Pharmaceutical composition for the prevention and treatment of obesity. delete delete delete Contains processed extracts of Panax ginseng or Panax quinquefolia from which ginsenosides (Rg3 + Rg5 + Rk1) / (Rb1 + Rb2 + Rc + Rd) have been increased to an active ingredient of 1.0 Health functional food for the prevention and improvement of obesity. delete delete

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