The Expression Of Mas Receptor, TGF-β1/Smad3，CTGF On Hepatic Stellate Cell Induced By Ang（1-7）

Objective:To observe the expression of Mas receptor 、 transforming growth factor beta1(TGF- beta 1) 、 Smad3 、 CTGF on the hepatic stellate cells which induced by angiotensin Ⅱ(Ang Ⅱ) and then treated with the angiotensin(1-7)(Ang1-7),we cultivated hepatic stellate cells in vitro to discusses the role of Ang(1-7) and its possible mechanism in the process of liver fibrosis and then provide theoretical basis for clinical treatment of liver fibrosis.Methods:Rat hepatic stellate cells(HSC- T6) were divided into six groups: normal control group、three concentrations Ang Ⅱ treatment groups、Ang Ⅱ + Ang(1-7)group、Ang Ⅱ + Ang(1-7) +A779 group(Mas receptor antagonist A779). When they were cultured 24 hours, we used the method of flow cytometry instrument(AnnexinV/PI staining) to detect each group cell’s apoptosis rate and at the same time we detected the expression of Mas receptor、TGF- beta 1、Smad3、CTGF mRNA and protein by the method of real- time PCR and Western Blotting.Results:(1) In Ang Ⅱ treatment group,the experssion of TGF- beta 1、Smad3、CTGF、Mas receptor mRNA and protein is raised(P < 0.05) compared with normal controlgroup.(2) In Ang Ⅱ + Ang(1-7) group, hepatic stellate cells’ apoptosis rate increased, while the expression of TGF- beta 1、Smad3、CTGF mRNA reduced(P <0.05), the expression of Mas receptor increased(P < 0.05) compared with Ang Ⅱtreatment group.(3) In Ang Ⅱ + Ang(1-7) + A779 group, hepatic stellate cells’ apoptosis rate、TGF- beta 1、Smad3、 CTGF mRNA expression increased, Mas receptor expression reduced(P < 0.05) compared with Ang Ⅱ + Ang(1-7) group.Conclusion:Ang Ⅱ can induce rat hepatic stellate cell activated and prompt the expression of TGF- beta 1、Smad3、CTGF. Ang(1-7) can increase the apoptosis of hepatic stellate cells induced by Ang Ⅱ and play a role of anti-liver fibrosis. And it exerts its antagonism role mainly through combination with Mas receptor, and its mechanism may be related to inhibit TGF- beta 1 / Smad3 signaling pathways.