Jie Cui, Meng Xue, Qian Xia
Apr 1, 2009
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Journal
The FASEB Journal
Abstract
Bicyclol is a novel antihepatitis drug with cytoprotective effects. The present study was to determine whether bicyclol played a protective role in myocardial ischemia and reperfusion. Myocytes isolated from adult male Sprague‐Dawley rats by enzymatic dissociation were subjected to 60 min anoxia and reoxygenation for 30 min. Trypan blue was used as the index of the viability of the isolated cardiomyocytes. Reactive oxygen species (ROS) generation and mitochondrial membrane potential were measured spectrophotofluorometrically with the fluorescent dye 2',7′‐dichlorfluorescin‐diacetate (DCFH‐DA) and tetramethyl‐rhodamine ethyl ester (TMRE) respectively. Absorbance at 520 nm was measured in isolated cardiac mitochondria exposed to 200 μM CaCl2 to show the mitochondrial permeability transition pore opening. In the isolated ventricular myocytes, pretreatment with bicyclol (1 μM) for 5 min increased the cell viability, and inhibited the increase intensity of DCFH‐DA and TMRE. The decrease of absorbance at 520 nm evoked by 200 μM CaCl2 was greatly inhibited by bicyclol. But the inhibition effect was attenuated by atractyloside (20 μM), inhibitor of mitochondrial permeability transition pore. The results indicate that bicyclol prevented cell death induced by simulated ischemia and reperfusion and the release of ROS. Bicyclol also inhibited the depolarization of the mitochondrial membrane induced by anoxia and reoxygenation. Bicyclol reduced Ca2+ induced mitochondrial swelling via inhibiting MPTP opening. We get that bicyclol is cardioprotective against ischemia and reperfusion, probably via inhibiting ROS generation and mitochondrial permeability transition pore opening.