Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling

AbstractBackground and aims Coronary heart disease is a major global health concern. Further, severity of this condition greatly influenced by myocardial ischemia/reperfusion (I/R) injury. Branched-chain amino acids (BCAAs) have cardioprotective effects against I/R via mammalian target rapamycin (mTOR) activity, wherein Leu considered to particularly regulate mTOR activation. However, the mechanism underlying activity not fully elucidated. Here, we aimed study signaling pathway cardioprotection mitochondrial function induced treatment. Methods results Cardiac myocytes isolated from adult male Wistar rats were incubated exposed simulated (SI/R) injury replacing air content. treated with subsequently, their survival rate was calculated. To elucidate function, immunoblots permeability transition pore examined. Cell decreased SI/R but improved 160 ?M (38.5 ± 3.6% vs. 64.5 4.2%, respectively, p < 0.001). Although (mTOR inhibitor) prevented effect Leu, wortmannin (PI3K did interfere effect. In addition, indicated that overexpression Opa-1 are ameliorated Leu-induced biogenesis. contrast, knockdown suppressed cardioprotection. Conclusion treatment critical in rendering exhibited BCAAs signaling. Furthermore, function.