Lipid-Lowering Effect of Ginkgo biloba Peptides on High-Fat Diet Induced Hyperlipidemia in Mice

This paper investigated the lipid-lowering effect of Ginkgo biloba peptides on high-fat diet induced hyperlipidemia in mice. Mice were randomly divided into six groups, including normal group, high-fat model group, Ginkgo biloba peptides low-dose (100 mg/kg), medium-dose (200 mg/kg), high-dose group (400 mg/kg) and positive control group (10 mg/kg simvastatin). A hyperlipidemia mice mode was established by feeding high-fat diet. Body weight, liver index, food intake, and apparent fat digestibility were measured. The kits were employed to determine the levels of the serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high density liptein cholesterol (HDL-C), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and the levels of the liver tissue total antioxidant capacity (T-AOC), total superoxide dismutase (T-SOD) and malondialdehyde (MDA). The atherogenic index (AI) and coronary heart index (CHI) were calculated. The results showed that the low, medium and high doses of Ginkgo biloba peptides significantly reduced the body weight and liver index (P<0.05), increased the apparent fat digestibility (P<0.05), had no significant effect on the food intake (P>0.05), down-regulated the TC, TG and LDL-C levels (P<0.05), up-regulated the HDL-C level, down-regulated the inflammatory cytokine IL-6 and TNF-α levels (P<0.05), reduced AI and CHI (P<0.05), promoted the T-AOC and T-SOD levels, and reduced the MDA level (P<0.05) as compared with the high-fat model group. No significant difference was found in liver index, food intake, apparent fat digestibility, TG, TC, HDL-C, CHI, IL-6, and TNF-α between the high-dose group and the positive control group (P>0.05). Ginkgo biloba peptides has an auxiliary lipid-lowering effect on high-fat diet induced hyperlipidemia in mice, and the underlying mechanisms is related to improving the body's antioxidant capacity and inhibiting the expression of pro-inflammatory cytokines.