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

• Main Authors: Han Zhong (Author), Hong Xin (Author), Li-Xin Wu (Author), Yi-Zhun Zhu (Author)
• Format: Book
• Published: Elsevier, 2010-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 1347-8613; 10.1254/jphs.10078FP
• Keywords: Therapeutics. Pharmacology; RM1-950
• Source: Journal of Pharmacological Sciences, Vol 114, Iss 4, Pp 399-408 (2010)

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. Keywords:: salidroside, ischemia, cardiomyocyte, apoptosis, reactive oxygen species