β-Sitosterol improves acute nephritis in rats by inhibiting inflammasome and activating autophagy

Abstract β-sitosterol is a compound found in many plants and has a variety of biological activities, including immunomodulatory and anti-inflammatory activities. The purpose of this study is to test its anti-inflammatory ability through a mouse model of acute nephritis. Methods: Acute nephritis mouse model was established by intravenous injection of antibodies. Pathological examination was used to test the therapeutic effect of β-sitosterol on model rats. Furthermore, the expression of related molecules was detected by ELASA. Results: β-sitosterol improved acute nephritis by repairing renal function, proteinuria and renal pathology, especially reducing cell crescents, neutrophil influx, glomerular fibrinoid necrosis and glomerulonephritis activity scores. β-sitosterol inhibits NLRP3 inflammasome mediated inflammasome initiation signal, enhances sirtuin 1 (SIRT1)/autophagy axis and inhibits the secretion of NLRP3 inflammasome. Conclusion: β-sitosterol represents a new drug candidate for the treatment of acute nephritis, which can reduce the kidney damage in model rats by enhancing the SIRT1/autophagy axis and reducing the activation of NLRP3 inflammasome.