Objective To study the role of TLR4 in angiotension Ⅱ(AngⅡ)-induced vascular remodeling of hypertensive mice.Methods Eighteen wild C57 mice were divided into control group,AngⅡgroup and TLR4 group(6 in each group).The mice were infused with AngⅡfor 7 days and injected with TLR4 through the tail vein to neutralize antibodies 2 days before AngⅡinfusion and 7 days after AngⅡinfusion.Expressions of ET-1,α-SMA,PCNA,ICAM-1 and CD69 were detected by immunohistpchemistry and flow cytometry,respectively.Results The blood pressure and expression levels of ET-1,ICAM-1 and CD69 were significantly higher whereas the expression level of α-SMA was significantly lower in AngⅡgroup than in control group(P<0.05,P<0.01).The blood pressure and expression levels of ET-1,PCNA,ICAM-1 and CD69 were significantly lower whereas the expression level of α-SMA was significantly higher in TLR4 group than in AngⅡgroup(P<0.05,P<0.01).Conclusion TLR4 participates in AngⅡ-induced vascular remodeling of hypertensive mice by mediating inflammatory reactions.

Objective To study the role of TLR4 in angiotension II(Ang II )-induced cardiac fibrosis in hypertensive mice.Methods Eighteen male wild-type mice were divided into blank control group,Ang II group,and TLR4 blocking group(6 in each group).A hypertension model was established by Ang II perfusion with a micropump.Blood pressure was measured in mice through the tail artey cuff and heart function of the mice was tested by echocardiacgraphy after injection of TLR4 neutralizing antibodies through the tail artery.Cardiac fibrosis in the mice was observed with immunohistochemical and Masson staining.Expressions of myocardial interleukin 1(3 and mononuclear cell chemotactic protein 1 mRNA were detected by RT-PCR.Results The blood pressure was lower,the left ventricular wall was thinner,the inner diameter of left ventricule at the end-diastolic phase was larger,the number of infiltated Mac-2 positive macrphygocytes was less,the expression level of interleukin 1βand mononuclear cell chemotactic protein 1 mRNA was lower,and the fibrosis of myocardial interstitium and peripheral blood vessels was milder in TLR4 blocking group than in Ang U group(P<0.05).Conclusion TLR4 participates in Ang II -induced cardiac fibrosis in hypertensive mice by mediating inflammatory reactions.