Protective mechanism of shenmai on myocardial ischemia-reperfusion through the energy metabolism pathway.

Shenmai (SM) injection has been reported to attenuate ischemia-reperfusion (I/R) injury, but its effect on energy metabolism during I/R and the underlying mechanism remain unknown. To explore the protective mechanism of SM on ischemic cardiomyopathy, primary cardiomyocytes from SD rats were treated with SM, total saponins of Panax ginseng (TSPG), L-carnitine (LC) and trimetazidine (TMZ). Changes in glucose, free fatty acids (FFAs), pyruvic acid (PA), lactic acid (LA) and intracellular ATP capacity were observed with the appropriate assays. For each treatment group, the key enzymes and transporters of myocardial energy metabolism were detected and compared via Western blot. Furthermore, impairments after I/R were assessed by examining cardiomyocyte apoptosis and LDH and PK activity in the culture medium. Our results indicated that SM and TSPG markedly alleviated the decrease in key enzymes and transporters and the utilization of metabolic substrates following I/R, while SM prevented aberrant apoptosis and restored the depleted ATP resulting from I/R. Notably, the effects of SM were superior to those of its main components TSPG, LC and TMZ. Thus, the protective effect of SM in ischemic cardiomyopathy may be mediated by the upregulation of key enzymes and restoration of the depleted ATP content in the energy metabolism process.