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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

1
State Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing 210009, China
2
College of Pharmacy, Xinjiang Medical University, Urumqi 830011, China
3
Cancer Hospital Affiliated to Xinjiang Medical University, Urumqi 830011, China
4
Xinjiang Key Laboratory of Medical Animal Model Research, Clinical Medical Research Institute of the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, China
5
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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Abstract

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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