Abstract

Liver fibrosis is a kind of lesion caused by damaged hepatocytes that may contribute to diverse severe liver diseases if not treated promptly. MCPIP1 was a protein which could protect the liver from ischemia reperfusion and LPS induced inflammation response. But whether MCPIP1 could alleviate liver fibrosis was not revealed. In our research, we used CCl4 on rats to construct the liver fibrosis animal model. Moreover, TGF-β1 was used to induce LX2 cells so as to establish the fibrotic cell model. Then we detected the expression of MCPIP1 in these tissues and cells. After that, the cellular morphology of LX2 cells was observed and the levels of α-SMA, collagen I, desmin, E-cadherin, Slug, N-cadherin, p-Smad3, Smad3 and Smad4 in LX2 cells were detected with western-blotting. The results showed that the expression of MCPIP1 was decreased in the liver fibrosis tissues and that TGF-β1 induced LX2 cells. In addition, the shape of TGF-β1 induced LX2 cells to gradually become spindle shaped. Furthermore, the expression of α-SMA, collagen I, desmin, Slug, N-cadherin, p-Smad3 and Smad4 was enhanced in TGF-β1-induced LX2 cells. However, the levels of these proteins were further suppressed after the overexpression of MCPIP1. MCPIP1 alleviated liver fibrosis by inhibiting the TGF-β/Smad pathway and EMT which was induced by the TGF-β/Smad pathway.

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