Mechanism of Anti-Hepatic Fibrosis of TGF-beta 1/Smad Signaling Pathway Affected by Chymase Inhibitors
Mechanism of Anti-Hepatic Fibrosis of TGF-beta 1/Smad Signaling Pathway Affected by Chymase Inhibitors
复制标题
食糜酶抑制剂影响TGF-β1/Smad信号通路抗肝纤维化的机制
DOI：
10.1166/jbt.2020.2331
复制
发表时间：
2020
影响因子：
0.1
通讯作者：
Yin Ming-Shi
中科院分区：
文献类型：
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作者：
Han Xue-Ji;Chen Ning;Yin Ming-Shi
目的探讨食糜酶抑制剂（Chy-I）对肝纤维化大鼠肝组织的病理机制。方法采用四氯化碳建立模型组和食糜酶抑制剂组大鼠。食糜酶抑制剂组大鼠在建模过程中灌胃Chy-I（10 mg/kg/d）。检测食糜酶抑制剂诱导的大鼠肝组织病理变化，观察大鼠肝组织中TGF-β1、Smad3、Smad7 mRNA和蛋白表达量。结果与模型组相比，Chy-I组大鼠肝组织病理学明显改善。与正常组比较,肝组织中TGF-β1、Smad3 mRNA表达量和蛋白表达量显着升高,而Smad7 mRNA表达量和蛋白表达量显着降低(p<0 05)。与模型组比较,Chy-I组TGF-β1、Smad3 mRNA表达量和蛋白表达量显着下调,而Smad7 mRNA表达量和蛋白表达量显着上调。结论Chy-I通过多位点影响肝组织TGF-β1/Smad信号通路,发挥积极的阻断大鼠肝纤维化的作用。
ObjectiveThis study aims to investigate the pathological mechanism of chymase inhibitors (Chy-I) on liver tissue in rats with hepatic fibrosis.MethodsRats in the model group and chymase inhibitor group were established by using carbon tetrachloride. Rats in the chymase inhibitor group intragastrically received Chy-I (10 mg/kg/d) during the modeling. The pathological changes of rat liver tissues induced by chymase inhibitors were investigated, and the mRNA and protein expression of TGF-β1, Smad3 and Smad7 were observed in rat liver tissues.ResultsWhen compared to the model group, The results presented that the liver tissue pathology of rats had been significantly improved in the Chy-I group. When compared to the normal group, the mRNA expression level and protein expression level of TGF-β1 and Smad3 in liver tissues had significantly increased, but the mRNA expression level and protein expression level of Smad7 significantly decreased (p 0 05). When compared to the model group, the mRNA expression level and protein expression level of TGF-β1 and Smad3 was significantly downregulated, but the mRNA expression level and protein expression level of Smad7 was significantly upregulated in the Chy-I group.ConclusionChy-I plays an active role in blocking hepatic fibrosis in rats by affecting the TGF-β1/Smad signaling pathway in liver tissues through multiple sites.