title: Salidroside attenuates apoptosis in ischemic cardiomyocytes: a mechanism through a mitochondria-dependent pathway.
abstract: 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.
authors.affiliation: Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201203, China.
authors.forename: Han
authors.initials: H
authors.lastname: Zhong
authors.forename: Hong
authors.initials: H
authors.lastname: Xin
authors.forename: Li-Xin
authors.initials: LX
authors.lastname: Wu
authors.forename: Yi-Zhun
authors.initials: YZ
authors.lastname: Zhu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005960:Glucosides / Q000494:pharmacology* / Q000627:therapeutic use*; D008297:Male; D008564:Membrane Potentials; D008929:Mitochondria, Heart / Q000378:metabolism*; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000473:pathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D010636:Phenols / Q000494:pharmacology* / Q000627:therapeutic use*; D010766:Phosphorylation; D008517:Phytotherapy; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*; D029771:Rhodiola; D015854:Up-Regulation; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D005960:Glucosides; D010636:Phenols; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D051057:Proto-Oncogene Proteins c-akt; D053148:Caspase 3; C009172:rhodioloside