Key result
Salidroside pretreatment reduces cardiomyocyte and myocardial apoptosis in acute myocardial infarction models.
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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.
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Zhong et al. (2010) studied Acute myocardial infarction / myocardial ischemia (rat and cellular models). Salidroside vs. Control (untreated OGD cardiomyocytes and AMI rats) was evaluated on Cardiomyocyte viability and myocardial apoptosis. Salidroside pretreatment attenuated oxygen-glucose deprivation-induced cardiomyocyte apoptosis and reduced myocardial apoptosis in rats with acute myocardial infarction.
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