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Molecules 2016, 21(6), 683; doi:10.3390/molecules21060683

Clematichinenoside (AR) Attenuates Hypoxia/Reoxygenation-Induced H9c2 Cardiomyocyte Apoptosis via a Mitochondria-Mediated Signaling Pathway

State Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing 210009, China
College of Pharmacy, Xinjiang Medical University, Urumqi 830011, China
Cancer Hospital Affiliated to Xinjiang Medical University, Urumqi 830011, China
Xinjiang Key Laboratory of Medical Animal Model Research, Clinical Medical Research Institute of the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, China
Institute of Indigenous Medicine, University of Colombo, Rajagiriya 11600, Sri Lanka
Author to whom correspondence should be addressed.
Academic Editors: Atanas G. Atanasov, Karel Šmejkal and Elke Heiss
Received: 11 April 2016 / Revised: 8 May 2016 / Accepted: 20 May 2016 / Published: 30 May 2016
(This article belongs to the Special Issue Effects of Natural Products in the Context of Cardiometabolic Disease)
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Mitochondria-mediated cardiomyocyte apoptosis is involved in myocardial ischemia/reperfusion (MI/R) injury. Clematichinenoside (AR) is a triterpenoid saponin isolated from the roots of Clematis chinensis with antioxidant and anti-inflammatory cardioprotection effects against MI/R injury, yet the anti-apoptotic effect and underlying mechanisms of AR in MI/R injury remain unclear. We hypothesize that AR may improve mitochondrial function to inhibit MI/R-induced cardiomyocyte apoptosis. In this study, we replicated an in vitro H9c2 cardiomyocyte MI/R model by hypoxia/reoxygenation (H/R) treatment. The viability of H9c2 cardiomyocytes was determined by MTT assay; apoptosis was evaluated by flow cytometry and TUNEL experiments; mitochondrial permeability transition pore (mPTP) opening was analyzed by a calcein-cobalt quenching method; and mitochondrial membrane potential (ΔΨm) was detected by JC-1. Moreover, we used western blots to determine the mitochondrial cytochrome c translocation to cytosolic and the expression of caspase-3, Bcl-2, and Bax proteins. These results showed that the application of AR decreased the ratio of apoptosis and the extent of mPTP opening, but increased ΔΨm. AR also inhibited H/R-induced release of mitochondrial cytochrome c and decreased the expression of the caspase-3, Bax proteins. Conversely, it remarkably increased the expression of Bcl-2 protein. Taken together, these results revealed that AR protects H9c2 cardiomyocytes against H/R-induced apoptosis through mitochondrial-mediated apoptotic signaling pathway. View Full-Text
Keywords: clematichinenoside (AR); apoptosis; H9c2 cardiomyocytes; hypoxia/reoxygenation; mitochondria; signaling pathway clematichinenoside (AR); apoptosis; H9c2 cardiomyocytes; hypoxia/reoxygenation; mitochondria; signaling pathway

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Ding, H.; Han, R.; Chen, X.; Fang, W.; Liu, M.; Wang, X.; Wei, Q.; Kodithuwakku, N.D.; Li, Y. Clematichinenoside (AR) Attenuates Hypoxia/Reoxygenation-Induced H9c2 Cardiomyocyte Apoptosis via a Mitochondria-Mediated Signaling Pathway. Molecules 2016, 21, 683.

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