AMPK–Nrf2–mediated cardioprotection by luteolin in a murine model of endotoxic myocardial damage

Abstract

Multi-organ failure brought on by the body's aberrant reaction to microbial invasion is the hallmark of polymicrobial sepsis, a potentially fatal condition. The study aimed to elucidate the putative cardioprotective action of luteolin against endotoxic heart injury induced by experimental sepsis in mice. Experimental animals were divided in to four groups, each contain 6 mice. Cecal Ligation and Puncture, Sham, DMSO & luteolin-treated groups 50mg/kg IP, 1hour before Cecal Ligation and Puncture, after that animals were sacrificed 24 hours after Cecal Ligation and Puncture. Markers evaluated include, IL-1β, TNFα, TNF αr1, HO-1 F2-ISOPROSTANEMPO, CASPASE-11 & troponin by ELISA technique, histopathological study & PCR for gene expression of AMPK-Nrf2 was done. IL-1β, TNFα, TNFαr1, HO-1, MPO, CASPASE-11, F2-isoprostane, tissue mRNA expression of AMPK-Nrf22 genes were significantly altered in the luteolin-treated group compared to the CLP group (p<0.05). We conclude that Luteolin contains anti-inflammatory and anti-oxidative properties; we conclude that it has cardioprotective benefits. Additionally, luteolin demonstrated a cardioprotective impact by influencing the AMPK-Nrf2 genes' tissue mRNA expression.