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Schematic diagram of the proposed mechanisms underlying the protective effects of FA on oxidative stress, inflammation in macrophages and HSC activation during liver fibrosis. FA ameliorated CCl4-induced oxidative stress in hepatocytes, relieved LPS-induced inflammation in macrophages and alleviated TGF-β-induced fibrotic response in HSCs. The potential mechanism was that FA directly bound to and inhibited the activity of PTP1B, eventually leading to the phosphorylation of AMPK.
