Salvianolic Acid B On Apolipoprotein E-deficient Mice Atherosclerosis Intervention Effect

Objective: To observe the effect of Salvianolic acid B on atherosclerosis (AS) of apolipoprotein E-knockout (ApoE-/-) Mice. Methods: Seven weeks old ApoE-/- mice were divided randomly into Atorvastatin calcium group (ATO), Model group (MOD), Salvianolic acid B high dose group (SalBH), and Salvianolic acid B low dose group (SalBL). Meanwhile, take 10 healthy mice (C57BL/6 mice) with the same age and same genetic background to be the Normal group (NOR). At the 8th week with continuous intragastric administration, the aortas and hearts tissue were taken for HE and immunohistochemistry ICAM-1 stain in order to make morphological research. Results: 1.The result of pathomorphology suggested that the pathological changes of ApoE-/- mice's aortas and coronary arteries in MOD group were serious. The thickness of vessal walls were uneven,and the endomembranes were unsmooth,the plaques were thick, while the fabric caps were thin, the lipid cores were large. There are lots of foam cells and cholesterol crystal forming the atheromatous plaques, which were not sticking enough to the vessal walls. The pathological changes of SalBH,SalBL groups were obviously improved than MOD group. The arterial walls was thinner, most of the swelling endomembrane were like rete pegs. There just have a small quantity of foam cells and hardly see cholesterol crystal. The lipid plaques were sticking tightly with the vessal walls. Some of the samples had calcium mineralization, showing the plaques were relatively stable, and SalBH's effect was the best, even better than ATO. 2. Slice of immunohistochemistry stain shows that there is no manifest ICAM-1 express in NOR group, while in MOD group the ICAM-1 express is outstanding. In ATO and SalBL group, we could see ICAM-1 expree, but it is less than MOD. There are very little ICAM-1 express in SalBH group, and the colour is light. Conclusion: Salvianolic acid B can relieve the lesions of ApoE-/- mice'AS and stabilize the aortic lipid plaque, and it also can restrain the express of ICAM-1.