Salvia extract on hyperlipidemic hamster glucose and lipid metabolism in.docVIP

 PAGE \* MERGEFORMAT 9 Salvia extract on hyperlipidemic hamster glucose and lipid metabolism in Author: Wang Zhuo ZHU Bao-Long Xu Nannan Kim Jin Tang Fu Li Wen-Xiang Hu [Abstract] Objective To observe the Salvia extract (SM) on the high-fat hamster lipid and glucose metabolism and to explore its mechanism. Method of high fat diet-induced hyperlipidemia golden hamster model, set up the normal group, model group, simvastatin group (1 mg * kg-1), SM treatment group (4.5,9.0 g * kg-1). Once every two weeks testing of serum TC, TG, HDL-C and LDL-C levels. Sacrificed 49 d after the hamster, testing four targets lipids, blood glucose, ApoA1 / B, MDA level and SOD activity with the FFA. HE staining in rat liver disease. The results of SM significantly reduced high-fat hamster serum TC, TG, LDL-C, ApoB, MDA and FFA levels, slightly elevated blood glucose concentrations significantly increased SOD activity, while HDL-C and ApoA1 levels had no significant effect. HE staining showed that Danshen can improve the high-fat to fatty degeneration of rat liver cells. Conclusion SM can effectively regulate glucose and lipid metabolism fat in mice and its mechanism may be related to the decrease lipid-lowering ApoB and FFA levels and antioxidant function. [Keywords:] Salvia fat superoxide dismutase MDA apo free fatty acids Abstract: ObjectiveTo investigate the effects of the extracts of Salvia miltiorrhiza (SM) on metabolism of plasma lipid and glucose in the hyperlipidemic hamsters and the related mechanism.MethodsHyperlipidemic model was induced by high fat diet (HFD) in hamsters, and five groups were designed : normal control (NC), model control (MC), Simvastatin group (1.0 mg * kg-1), and SM groups (4.5, 9.0 g * kg-1). The levels of TC, TG, HDL-C, and LDL-C were determined every two weeks. After medication for 49 days, all hamsters were killed, and the levels of plasma TC, TG, HDL-C, LDL-C, glucose, ApoA1 / B, MDA, FFA and the activity of superoxide dismutase (SOD) wer