Study on the Lipid-lowering Effect and Potential Mechanism of the Couplet Medicines of Flastem Milkvetch Seed and Tribulus Terrestris on Hyperlipidemia Rats / 世界科学技术-中医药现代化

ABSTRACT

Objective: To explore the lipid-lowering effect and potential mechanism of the couplet medicines of Flastem Milkvetch Seed and Tribulus terrestris on hyperlipidemia rats. Methods: Forty-eight Sprague-Dawley rats were randomly divided into 6 groups, normal control group, high-fat model group, simvastatin group, Tribulus terrestris group, Flastem Milkvetch Seed group, and couplet medicines of Flastem Milkvetch Seed and Tribulus terrestris group, with 8 rats in each group. The normal control group was fed with basal diet, and the other groups were fed with high-fat diet to establish a hyperlipidemia rat model. At the same time, different group rats were treated with different drug respectively. 6 weeks later, the body weight and visceral index of the rats were measured. Levels of serum cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), and low density lipoprotein cholesterol (LDL-C) were detected by automatic biochemical analyzer. The mRNA and protein expression of HMG coenzyme A reductase (HMGCR), cholesterol 7-alpha hydroxy-lase (CYP7A1) and low density lipoprotein receptor (LDL-R) were detected by RT-PCR and western blot. Results: Compared with model group, the serum levels of TC, TG, and LDL-C were significantly decreased in all Chinese medicine groups, and the serum level of HDL-C was significantly increased in Flastem Milkvetch Seed group and couplet medicines of Flastem Milkvetch Seed and Tribulus terrestris group. Moreover, the mRNA and protein expression of HMGCR, CYP7A1, and LDL-R in rat liver also significantly increased in all Chinese medicine treatment groups. And couplet medicines of Flastem Milkvetch Seed and Tribulus terrestris group shows more significantly effect. Conclusion: Couplet medicines of Flastem Milkvetch Seed and Tribulus terrestris significantly regulate the serum lipid levels on hyperlipidemia rat model, and its mechanism may be related to the regulating expressions of HMGCR, CYP7A1, LDL-R gene.