Effects of TLR3 activator-poly (I∶C)on atherosclerotic plaque formation in ApoE-/-mice and its molecular mechanism
Abstract：Objective To investigate the effects of TLR3 activator-poly (I ∶ C) on atherosclerotic plaque formation in ApoE-/-mice and its molecular mechanism.Methods A total of 10 specific pathogen free(SPF) male ApoE-/-mice were randomly divided into model group and poly (I ∶ C)group,with 5 mice in each group.The mice in model group and poly (I ∶ C) group were fed with high fat diet and high fat diet + poly (I ∶C),respectively,and the other five C57BL/6J mice fed with normal diet C57BL/6J were served as control group.After 14-week feeding,all the mice were sacrificed,then the body weight,fiber-cap thickness,vascular intima-media thickness,TC,TG,LDL-C,HDL-C,NO,MDA,SOD,IL-6,IL-1β,TNF-oα,VCAM-1,ICAM-1,P-selection and the expression levels of TLR3,TRIF,p-p38,p-JNK and p-ERK were observed and compared among the three groups.Results The body weight in model group was significantly higher than that in control group(P ＜ 0.05),but there was no significant difference in body weight between model group and poly(I ∶ C) group (P ＞ 0.05).No aortic plaque formation was found in control group,however,obvious aortic plaque formation and increase of vascular intima-media thickness were found in model group (P ＜ 0.05).As compared with those in model group,the aortic plaque formation and vascular intima-media thickness were significantly decreased in poly (I ∶ C) group (P ＜ 0.05).As compared with those in control group,the levels of TC,TG,LDL-C,MDA,IL-6,IL-1β,TNF-α,VCAM-1,ICAM-1,P-selection and the expression levels of TLR3,TRIF,p-p38,p-JNK,p-ERK proteins in model group were significantly increased,however,the levels of HDL-C,NO,SOD were significantly decreased (P ＜ 0.05).As compared with those in model group,the tevels of TC,TG,LDL-C,MDA,IL-6,IL-1β,TNF-α and the expression levels of VCAM-1,ICAM-1,P-selection,TLR3,TRIF,p-p38,p-JNK,p-ERK proteins were significantly decreased in poly (I ∶ C) group,however,the levels of HDL-C,NO and SOD were significantly increased (P ＜ 0.05).Conclusion TLR3 activator-poly (I ∶ C) can inhibit atherogenesis and relieve AS lesion in ApoE-/-mice by inhibiting the activation of TLR3/TRIF signal pathway and decreasing inflammatory factors release.
Keywords：Toll-like acceptor 3atherosclerosisApoE genetic flaw
Publication Date：2017-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：4( 3712-3715 )