Salidroside attenuates apoptosis in ischemic cardiomyocytes: A mechanism through a mitochondria-dependent pathway

In the present study,we investigated cardioprotective effects of salidroside,isolated from rhodiola rosea l,on oxygen-glucose deprivation (ogd)-induced cardiomyocyte death and ischemic injury evoked by acute myocardial infarction (ami) in rats. pretreatment with salidroside notably ameliorated cell viability losses in a dose-dependant manner and in parallel it alleviated morphologic injury detected by electron microscopy. mechanistically,diminished ogd-induced cardiomyocyte apoptosis was shown in salidroside-pretreated cardiomyocytes,in accordance with minimal reactive oxygen species (ros) burst. moreover,salidroside markedly upregulated the bcl-2/bax ratio and preserved mitochondrial transmembrane potential (δψm). salidroside administration also inhibited myocardial apoptosis in ami rats by increasing phosphorylation of akt and decreasing activation of caspase-3. these findings suggest that salidroside reduced ischemia-mediated myocardial damage. salidroside therefore has potential to be a promising drug for preventing and treating myocardial ischemic diseases. ©2010 the japanese pharmacological society.