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Nonalcoholic steatohepatitis (NASH)-related liver fibrosis has been suggested to be a physiological consequence of chronic hepatic injury, necrosis, inflammation and unbalanced intrahepatic lipid metabolism. Accumulated evidence demonstrates that inducible nitric oxide synthase (iNOS) is highly expressed in advanced liver fibrosis, and the knockout of iNOS inhibits the progression of hepatic fibrosis. In our previous study, ()--(3-chlorophenyl)-2-(4-((2,4-dioxothiazolidin-5-ylidene)methyl)phenoxy)acetamide (SKLB023), a novel small-molecule inhibitor of iNOS, blocked joint inflammation and cartilage destruction in arthritis.

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