SIRT2 regulates oxidative stress response in liver fibrosis mice through the NLRP3 inflammasome pathway

Abstract Liver fibrosis is a crucial step in the progression of various chronic liver diseases to cirrhosis, which can affect the prognosis of chronic liver diseases. The NAD+ dependent deacetylase sirtuins family member SIRT2 can regulate the inflammatory corpuscular pathway in pathological processes, but its related mechanism is not yet clear. This study established liver fibrosis models in wild-type and SIRT2 knockout mice, and evaluated their effects on liver homeostasis using immunoblotting, immunofluorescence, and histopathological staining methods. The results indicate that the deletion of the SIRT2 gene enhances NLRP3 acetylation, activates the NLRP3 inflammasome pathway, and accelerates oxidative stress. These findings suggest that SIRT2 may be a potential target for regulating liver fibrosis and restoring health.