Effects of TLR3 activator-poly(I∶C)on vulnerable plaques of atherosclerosis and neovascularization in plaque of mice with ApoE-/-

doi:10.3969/j.issn.1002-7386.2018.13.001

Abstract：Objective To observe the effects of Toll-like receptor 3 ( TLR3 ) activator-poly ( I∶ C) on vulnerable plaques of atherosclerosis and neovascularization in plaque of mice with ApoE-/ -,and to explore the action mechanism of poly (I∶C)in anti-atherosclerosis. Methods A total of 10 specific pathogen free(SPF)male mice with ApoE-/ -were divided randomly into model group and poly(I∶C) group,with 5 mice in each group. The mice in model group were fed with high fat diet,however, the mice in poly(I∶C)group were fed with high fat diet+poly(I∶C). After 14-week feeding,the mice were sacrificed,and the contents of lipoid vesicles were detected by HE staining. The type andtype Ⅲ collagenous fibers were measured by Movat staining. The macrophages counts ,smooth muscle cells and intraplaque microvessel density were detected by immuneohistochemistry staining, and the plaque vulnerability index was evaluated. The apoptosis area and apoptosis cells in plaques were observed by TUNEL method,and the apoptosis index was calculated. The expression levels of MMP-2,TIMP-1, Bax,Bcl-2 and P53 mRNA and proteins were detected by Real time-PCR and Western blot, respectively. Results As compared with those in model group,the contents of lipoid vesicles,macrophages counts,the apoptosis area,apoptosis index, neovessels and the expression levels of MMP-2,Bax and P53 mRNA and proteins were significantly decreased in poly( I∶C) group,however,the contents of type Ⅰ and type Ⅲ collagenous fibers,smooth muscle cells, the expression levels of TIMP-1, Bcl-2 mRNA and proteins as well as the plaque vulnerability index were significantly decreased in poly( I∶C) group ( P ＜0.05).Conclusion TLR3 activator-poly(I∶C)can effectively reduce intraplaque foam cells,macrophages and microvessel density and increasetype Ⅰ and type Ⅲ collagenous fibers and smooth muscle cells,moreover,which can inhibit cell apoptosis by regulating the expression levels of Bax,Bcl-2 and P53 proteins,so as to increase the stability of the atherosclerosis plaque in ApoE/ mice.