Journal of Jilin University Medicine Edition ›› 2017, Vol. 43 ›› Issue (01): 16-20.doi: 10.13481/j.1671-587x.20170104

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Regulatory effect of direct renin inhibitor aliskiren on epithelial-mesenchymal transition of renal fibrosis mice

DENG Haiyue, YU Fang, JIANG Hong   

  1. Department of Pediatrics, First Affiliated Hospital, China Medical University, Shenyang 110001, China
  • Received:2016-03-05 Online:2017-01-28 Published:2017-02-08

Abstract:

Objective: To explore the regulatory effect of direct renin inhibitor aliskiren on epithelial-mesenchymal transition(EMT) of the renal fibrosis mice induced by unilateral ureteral occlusion,and to clarify its mechanisms of inhibiting renal fibrosis.Methods: Twenty-four ICR mice were divided into sham group,model group, and aliskiren intervention group. The renal fibrosis models were established by unilateral ureteral occlusion.The pathohistomorphology of renal interstitial fibrosis was observed by HE staining.The collagen protein expression in renal interstitial was observed by Masson staining.The α-smooth muscle actin(α-SMA) expression in the cytoplasm was observed by immnocytochemical staining.The protein expression levels of E-cadherin (E-cad), α-SMA,and type Ⅰ collagen(Col Ⅰ) in the kidney tissue of the mice were detected by Western blotting method.Results: The mouse models of renal fibrosis were successfully produced by unilateral ureteral occlusion.The HE staining and Masson staining results showed that the degree of mouse renal interstitial fibrosis in alikiren intervention group was decreased and the expression level of collagen was reduced compared with model group.The immnocytochemical staining results showed that the expression of α-SMA in renal interstitial fibrosis area in alikiren intervention group was obviously reduced compared with model group.The results of Western blotting methods showed that the expression levels of α-SMA and Col Ⅰ in model group were increased to 1.79 folds and 1.95 folds compared with sham group(P<0.05),while the expression level of E-cad was decreased to 37.23%(P<0.05);the expressions levels of α-SMA and Col Ⅰ were decreased to 63.72% and 65.54% compared with model group(P<0.05),while the expression level of E-cad was increased to 2.1 folds(P<0.05).Conclusion: Aliskiren can inhibit the EMT of renal fibrosis produced by unilateral ureteral occlusion via up-regulation of E-cad expression and down-regulation of expressions of α-SMA and Col Ⅰ.

Key words: α-smooth muscle actin, aliskiren, epithelial-mesenchymal transition, E-cadherin, kidney fibrosis

CLC Number: 

  • R-332