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.
Highlights
Ischemia/reperfusion is associated with thrombolysis, angioplasty and coronary bypass surgery which relieve myocardial ischemia, but simultaneously cause further damage to myocardial tissue, which is known as myocardial ischemia/reperfusion (MI/R) injury [1]
During MI/R injury, cardiomyocytes undergo apoptosis which results in ischemia/reperfusion myocardial contractile dysfunction, hypertrophy which is[3,4], known as myocardial (MI/R)
Resultsin H9c2 cardiomyocytes against H/R injury in a concentration-dependent manner
Summary
Ischemia/reperfusion is associated with thrombolysis, angioplasty and coronary bypass surgery which relieve myocardial ischemia, but simultaneously cause further damage to myocardial tissue, which is known as myocardial ischemia/reperfusion (MI/R) injury [1]. During MI/R injury, cardiomyocytes undergo apoptosis which results in ischemia/reperfusion myocardial contractile dysfunction, hypertrophy which is[3,4], known as myocardial (MI/R). MI/R injury is one of the deathand reparative of which further increase myocardial injury, and leads to cardiac threats infibrosis, various all cardiovascular diseases [2]. MI/R injury, cardiomyocytes undergo apoptosis [3,4], which results in myocardial contractile compensatoryprocesses hypertrophy and reparative dysfunction [5]. Of the key pathological in MI/R injury and which further increase myocardial and to cardiac dysfunctionthe thefibrosis, amountallofofapoptosis determines the severityinjury, of MI/R injury [6].leads.
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