Salidroside Attenuates Apoptosis in Ischemic Cardiomyocytes: a Mechanism Through a Mitochondria-Dependent Pathway

  • Zhong Han
    Department of Pharmacology, School of Pharmacy, Fudan University, China
  • Xin Hong
    Department of Pharmacology, School of Pharmacy, Fudan University, China
  • Wu Li-Xin
    Department of Pharmacology, School of Pharmacy, Fudan University, China
  • Zhu Yi-Zhun
    Department of Pharmacology, School of Pharmacy, Fudan University, China

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説明

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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