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Shikonin attenuates acetaminophen-induced acute liver injury via inhibition of oxidative stress and inflammation

In an immunocompetent mouse model of hepatitis B virus (HBV) infection, SFN treatment significantly promoted the repolarization of macrophages towards the antitumoral M1 phenotype, as evidenced by increased expression of Cd86 and iNOS, and inhibited the expression of Arg1

The defect disappears several days earlier compared to the untreated group and other possible supportive therapies