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 sandroside-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 (Delta Psi m) 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