Icariin improves hypertensive renal fibrosis and injury through Cx32-Nox4 signaling pathway
AIM:To investigate the effect of icari-in on renal fibrosis and injury in hypertension through Cx32-Nox4 signaling pathway.METHODS:Models of hypertensive nephropathy(HN)were es-tablished in spontaneously hypertensive rats(SHRs).The experiment was divided into 4 groups:normal control group(WKY rats),model group(SHR),icariin 10 mg·kg-1·d-1 group(icariin once dai-ly),icariin 30 mg·kg-1·d-1 group(icariin once daily),n=10.The expression of fibrosis-related proteins was detected in vivo.NRK-52E cells exposed to An-gⅡ were selected to observe the effects of icariin on kidney injury.Extracellular matrix(ECM)levels,including α-smooth muscle actin(α-SMA),collagenⅠ(Col-Ⅰ)and fibronectin(FN)expression were mea-sured by Western blot and immunohistochemistry.The expressions of oxidative stress markers includ-ing superoxide dismutase(SOD)and malondialde-hyde(MDA)were determined by the test kit.RE-SULTS:Icariin reduced renal fibrosis in SHR rats in vivo.Icariin down-regulated the expression of α-SMA,FN,and Col-Ⅰ and protected hypertension-damaged kidney tissue from progressive fibrosis(P＜0.05).Icariin increased the total SOD activity and decrease the MDA level in kidney and serum of SHR rats(P＜0.05).In addition,icariin increased the expression of Cx32 and decreased the expression of Nox4 in the kidneys of SHR rats(P＜0.05).Icariin had a protective effect on AngⅡ-mediated NRK-52E cell damage and fibrosis.CONCLUSION:Icariin can improve renal tubulointerstitial fibrosis and delay the progression of HN.Renal protection may be at-tributed to the regulation of oxidative stress medi-ated by the Cx32-Nox4 signaling pathway.
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