Mechanisms of the prevention and inhibition of the progression and development of non‐alcoholic steatohepatitis by genetic and pharmacological decoy receptor 3 supplementation

Treatment of non‐alcoholic steatohepatitis (NASH) is difficult due to the absence of a proven treatment and its comprehensive mechanisms. In the NASH animal model, upregulated hepatic inflammation and oxidative stress, with the resultant M1 polarization of macrophages as well as imbalanced adipocytokines, all accelerate NASH progression. As a member of the tumor necrosis factor receptor superfamily, decoy receptor 3 (DcR3) not only neutralizes the death ligands, but also performs immune modulations. In this study, we aimed to investigate the possible non‐decoy effects of DcR3 on diet‐induced NASH mice.

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