Protective Effects And Mechanism Of Liuwei Dihuang Pills On Hyperlipidemic Rats

Objective Observation of LWDHW in hyperlipidemia rats blood lipid, blood glucose, blood vessel related cytokines, aortic morphology and vascular adiponectin, adiponectin receptor expression of mRNA; Preliminarily determine the protective effect of LWDHW on Vascular in the experimental hyperlipidemic rats and its possible mechanisms; providing reference for the application of LWDHW in the prevention and treatment of cardiovascular disease.Methods Forty male Wistar rats were randomly divided into normal control group10rats,30rats in model group.The experimental model rats with hyperlipidemia were established by feeding high fat diet for8weeks later,the model group was divided into the model group, LWDHW-treated group and Simvastatin-treated group.Continuous intragastric administration for8weeks, we observe the protective effects of LWDHW on serum lipid in rat with hyperlipidemia, the level of serum total cholesterol(TC), Triglyceride(TG), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol(LDL-C), nitric oxide(NO), nitric oxidesynthase(NOS), endothelin(ET), interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)were measured. The aorta was taken for pathologic analysis by hematoxylin eosine (HE) staining. Serum adiponectin was detected by ELISA. The mRNA and protein expression of both AdipoRl and AdipoR2on the aorta was assayed by using RT-PCR and Western boltting. All experimental data are processed using statistical software SPSS16.0, represented by(x±s), comparisons between groups were tested by T test, P<0.05as the difference is statistically significant.Results1. Induced by high fat diet hyperlipidemia model and human hyperlipidemia with similar characteristics, can be used to study of hyperlipidemia.2. LWDHW group rats serum LDL-C was significantly lower than the model group (P<0.05).while TC,TG and HDL-C no significant differences. Compared with LWDHW group, the model group could remarkably decrease the serum NO and NOS. Compared with the model group, the LWDH ET-1,IL-6,TNF-α levers abnormally decreased and serum adiponectin lever increased. It showed that LWDHW can regulate lipid metabolism disorders; it can increasing plasm levels of NO and NOS, and decreasing of ET-1. 3. The observation of microscope:the normal group rat thoracic aortic wall structural integrity, its intimal smooth, smooth muscle cells arranged regularly, even without atrophy; Compared with the normal group, the thoracic aortic wall thickening of the intima of model group rats, the proliferation of smooth muscle cells, arranged in disorder; Simvastatin-treated group and LWDHW group was obviously pathological changes. The results suggest that LWDHW might significantly inhibit Aortic intimal thickening and vascular smooth muscle cells proliferation induced by high fat diet.4. According to the results of RT-PCR and Western Blotting, LWDHW could significantly increase the AdipoRl and AdipoR2mRNA expressions on the aorta in rat with hyperlipidemia. The expression of AdipoRl more than AdipoR2.Conclusion:Induced by high fat diet hyperlipidemia model and human hyperlipidemia with similar characteristics,can be used to research hyperlipidemia and its complications. LWDHW can reduce blood fat, improve endothelial function, inhibite the inflammatory reaction, has a protective effect on the aorta in hyperlipidemia rats. Its mechanism may be associated with increased serum adiponectin levels or raised adiponectin receptors (AdipoRl and AdipoR2) expression and so on, so as to protect the vascular function. Adiponectin research may provide a new theoretical basis for the prevention and treatment of hyperlipidmeic, lipid metabolic disorder and insulin resistance.