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Ginsenoside Rd attenuates myocardial ischemia/reperfusion injury via Akt/GSK-3β signaling and inhibition of the mitochondria-dependent apoptotic pathway.
PLoS One. 2013; 8(8):e70956.Plos

Abstract

Evidence suggests Ginsenoside Rd (GSRd), a biologically active extract from the medical plant Panax Ginseng, exerts antioxidant effect, decreasing reactive oxygen species (ROS) formation. Current study determined the effect of GSRd on myocardial ischemia/reperfusion (MI/R) injury (a pathological condition where ROS production is significantly increased) and investigated the underlying mechanisms. The current study utilized an in vivo rat model of MI/R injury and an in vitro neonatal rat cardiomyocyte (NRC) model of simulated ischemia/reperfusion (SI/R) injury. Infarct size was measured by Evans blue/TTC double staining. NRC injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. ROS accumulation and apoptosis were assessed by flow cytometry. Mitochondrial membrane potential (MMP) was determined by 5, 5', 6, 6'-tetrachloro-1, 1', 3, 3'-tetrathylbenzimidazol carbocyanine iodide (JC-1). Cytosolic translocation of mitochondrial cytochrome c and expression of caspase-9, caspase-3, Bcl-2 family proteins, and phosphorylated Akt and GSK-3β were determined by western blot. Pretreatment with GSRd (50 mg/kg) significantly augmented rat cardiac function, as evidenced by increased left ventricular ejection fraction (LVEF) and ±dP/dt. GSRd reduced myocardial infarct size, apoptotic cell death, and blood creatine kinase/lactate dehydrogenase levels after MI/R. In NRCs, GSRd (10 µM) inhibited SI/R-induced ROS generation (P<0.01), decreased cellular apoptosis, stabilized the mitochondrial membrane potential (MMP), and attenuated cytosolic translocation of mitochondrial cytochrome c. GSRd inhibited activation of caspase-9 and caspase-3, increased the phosphorylated Akt and GSK-3β, and increased the Bcl-2/Bax ratio. Together, these data demonstrate GSRd mediated cardioprotective effect against MI/R-induced apoptosis via a mitochondrial-dependent apoptotic pathway.

Authors+Show Affiliations

Department of Physiology, Fourth Military Medical University, Xi'an, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23976968

Citation

Wang, Yang, et al. "Ginsenoside Rd Attenuates Myocardial Ischemia/reperfusion Injury Via Akt/GSK-3β Signaling and Inhibition of the Mitochondria-dependent Apoptotic Pathway." PloS One, vol. 8, no. 8, 2013, pp. e70956.
Wang Y, Li X, Wang X, et al. Ginsenoside Rd attenuates myocardial ischemia/reperfusion injury via Akt/GSK-3β signaling and inhibition of the mitochondria-dependent apoptotic pathway. PLoS ONE. 2013;8(8):e70956.
Wang, Y., Li, X., Wang, X., Lau, W., Wang, Y., Xing, Y., Zhang, X., Ma, X., & Gao, F. (2013). Ginsenoside Rd attenuates myocardial ischemia/reperfusion injury via Akt/GSK-3β signaling and inhibition of the mitochondria-dependent apoptotic pathway. PloS One, 8(8), e70956. https://doi.org/10.1371/journal.pone.0070956
Wang Y, et al. Ginsenoside Rd Attenuates Myocardial Ischemia/reperfusion Injury Via Akt/GSK-3β Signaling and Inhibition of the Mitochondria-dependent Apoptotic Pathway. PLoS ONE. 2013;8(8):e70956. PubMed PMID: 23976968.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ginsenoside Rd attenuates myocardial ischemia/reperfusion injury via Akt/GSK-3β signaling and inhibition of the mitochondria-dependent apoptotic pathway. AU - Wang,Yang, AU - Li,Xu, AU - Wang,Xiaoliang, AU - Lau,Waynebond, AU - Wang,Yajing, AU - Xing,Yuan, AU - Zhang,Xing, AU - Ma,Xinliang, AU - Gao,Feng, Y1 - 2013/08/16/ PY - 2013/05/02/received PY - 2013/06/24/accepted PY - 2013/8/27/entrez PY - 2013/8/27/pubmed PY - 2014/4/9/medline SP - e70956 EP - e70956 JF - PloS one JO - PLoS ONE VL - 8 IS - 8 N2 - Evidence suggests Ginsenoside Rd (GSRd), a biologically active extract from the medical plant Panax Ginseng, exerts antioxidant effect, decreasing reactive oxygen species (ROS) formation. Current study determined the effect of GSRd on myocardial ischemia/reperfusion (MI/R) injury (a pathological condition where ROS production is significantly increased) and investigated the underlying mechanisms. The current study utilized an in vivo rat model of MI/R injury and an in vitro neonatal rat cardiomyocyte (NRC) model of simulated ischemia/reperfusion (SI/R) injury. Infarct size was measured by Evans blue/TTC double staining. NRC injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. ROS accumulation and apoptosis were assessed by flow cytometry. Mitochondrial membrane potential (MMP) was determined by 5, 5', 6, 6'-tetrachloro-1, 1', 3, 3'-tetrathylbenzimidazol carbocyanine iodide (JC-1). Cytosolic translocation of mitochondrial cytochrome c and expression of caspase-9, caspase-3, Bcl-2 family proteins, and phosphorylated Akt and GSK-3β were determined by western blot. Pretreatment with GSRd (50 mg/kg) significantly augmented rat cardiac function, as evidenced by increased left ventricular ejection fraction (LVEF) and ±dP/dt. GSRd reduced myocardial infarct size, apoptotic cell death, and blood creatine kinase/lactate dehydrogenase levels after MI/R. In NRCs, GSRd (10 µM) inhibited SI/R-induced ROS generation (P<0.01), decreased cellular apoptosis, stabilized the mitochondrial membrane potential (MMP), and attenuated cytosolic translocation of mitochondrial cytochrome c. GSRd inhibited activation of caspase-9 and caspase-3, increased the phosphorylated Akt and GSK-3β, and increased the Bcl-2/Bax ratio. Together, these data demonstrate GSRd mediated cardioprotective effect against MI/R-induced apoptosis via a mitochondrial-dependent apoptotic pathway. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/23976968/Ginsenoside_Rd_attenuates_myocardial_ischemia/reperfusion_injury_via_Akt/GSK_3β_signaling_and_inhibition_of_the_mitochondria_dependent_apoptotic_pathway_ L2 - http://dx.plos.org/10.1371/journal.pone.0070956 DB - PRIME DP - Unbound Medicine ER -