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. 2020 Jul 31;11:1038. doi: 10.3389/fphar.2020.01038

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Copyright © 2020 Li, Leng, Jiang, Wang, Luo, Zhang, Chen, Wang, Wang, Yue, Shen, Zhou, Shi and Xie

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Metformin reduces fibrosis in HConFs pretreated by TGF-β2 via activating AMPK/Nrf2 axis. (A–B) AICAR or metformin could increase the levels of p-Nrf2(S40), Nrf2 and p-AMPK in HConFs after TGF-β2 precondition for 24 h. (C) Cell cycle was tested and quantization of the rates in HConFs cells. Compound C or ML385 could reverse the inhibition of metformin on HConFs’ proliferation. (D–F) Cell cycle relative proteins/genes (CDK4, CyclinD1, P21 and P27) were detected by qRT-PCR/western blotting. (G–I) Antioxidant defense relative protein/genes γ-GCS, SOD1/2 and (J–L) fibrotic proteins/genes collagen-1, fibronectin, α-SMA level in HConFs treated by metformin with/without Compound C (10 μmol/L) or ML385 (10 mM) treatment for 24 h. MET = metformin, n = 3. All data shown as mean values ± SD. **^/## and ***^/### denote P < 0.01 and P < 0.001, respectively.