Study On The Mechanism Of Ginsenoside Re Improving Lipid Metabolism

[Objective] To study the effect and mechanism of ginsenoside Re on lipid metabolism in db/db mice.[Methods]18male db/db mice were randomly allocated to two groups, including vehicle group and Re treatment group. According to their assigned group, they were injected vehicle or Re intraperitoneally. Body weight and food intake of db/db mice were recorded daily. The liver, muscle and adipose tissues of the mice were removed at the end of animal experiment, according to defined anatomical landmarks, and frozen at-80℃refrigerator for further studies. Weights of the left side epididymal and subcutaneous adipose tissues were recorded. Serum levels of total cholesterol (TC) and triglyceride (TG) were determined by Elisa assay kits. The liver and adipose tissues were homogenized for RNA and protein extraction for real-time PCR and western blot test, which were performed for investigation of the molecular mechanisms of Re on lipid metabolism.[Results] There were no significant difference of average daily food intake between two groups. But Re notably inhibited the body weight gain in Re treatment group compared with vehicle group (p<0.05). And the weight of liver and epididymal adipose tissues, subcutaneous adipose tissues in Re treatment group were significantly lower than vehicle group. As for the circulating levels of TG and TC, they were significantly decreased in Re treatment group when compared with vehicle group. The hepatic TG level measured by Folch method in Re treatment group was statistically less than which in vehicle group. HE showed the hepatic lipid droplet was obviously less in Re treatment group than which in vehicle group. The real-time PCR showed that mRNA of genes related to lipid metabolism were statistically different between two groups. Western-blot determined that hepatic P-AMPK pathway was activated in Re treatment group.[Conclusion] Ginsenoside Re can inhibit db/db mice body weight gain without influencing food intake. Re significantly improved dyslipidemia in db/db mice, which, was partly putatively through activation of AMPK pathway.