SCM-198 Can Regulate Autophagy Through the Bax/Bcl-2/TLR4 Pathway to Alleviate Renal Ischemia-Reperfusion Injury

Abstract

Renal ischemia-reperfusion (I/R) injury is frequently observed in several clinical cases. In this study, we want to investigate that SCM-198 attenuates renal injury in the renal I/R model and find out the possible mechanisms. Wistar albino 40 male rats were classified into four groups (n=10): control, DMSO, I/R, and SCM-198 30 mg/kg. In the group 4, SCM-198 was administered intraperitoneally once at the doses of 30 mg/kg following the reperfusion. Glomerular associated proteins (PCX), tubular damage factors (NGAL, KIM-1), blood urea nitrogen (BUN), serum creatinine, inflammatory cytokines (IL-1 beta, IL-18, and TNF-alpha), Bax/Bcl-2, TLR4, LC3B, and Beclin-1 were evaluated. SCM-198 played an essential role in mitigating kidney damage. SCM-198 alleviated tubular damage and decreased IL-1 beta, IL-18, and TNF-alpha levels. SCM-198 reduced the apoptosis marker Bax/Bcl-2 ratio, immune system protein TLR4, and autophagy proteins LC3B and Beclin-1. In brief, our results support the notion that SCM-198 has protective effects on I/R-induced renal injury. SCM-198 therapy may be a new alternative for the prevention and treatment of renal I/R injury.