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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

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This would contradict the hypothesis of the role of peroxynitrite as the key oxidant in APAP pathophysiology and would also be inconsistent with the limited LPO

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