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The Role of Sulfur Dioxide in the Regulation of Mitochondrion-Related Cardiomyocyte Apoptosis in Rats with Isopropylarterenol-Induced Myocardial Injury
Department of Pediatrics, Peking University First Hospital, Xi'an Men Str. No. 1, West District, Beijing 100034, China
Department of Medical and Health Sciences, Linköping University, Linköping 58183, Sweden
Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100191, China
Department of Physiology and Pathophysiology, Health Sciences Center, Peking University, Beijing 100191, China
* Author to whom correspondence should be addressed.
Received: 5 March 2013; in revised form: 24 April 2013 / Accepted: 9 May 2013 / Published: 21 May 2013
Abstract: The authors investigated the regulatory effects of sulfur dioxide (SO2) on myocardial injury induced by isopropylarterenol (ISO) hydrochloride and its mechanisms. Wistar rats were divided into four groups: control group, ISO group, ISO plus SO2 group, and SO2 only group. Cardiac function was measured and cardiomyocyte apoptosis was detected. Bcl-2, bax and cytochrome c (cytc) expressions, and caspase-9 and caspase-3 activities in the left ventricular tissues were examined in the rats. The opening status of myocardial mitochondrial permeability transition pore (MPTP) and membrane potential were analyzed. The results showed that ISO-treated rats developed heart dysfunction and cardiac injury. Furthermore, cardiomyocyte apoptosis in the left ventricular tissues was augmented, left ventricular tissue bcl-2 expression was down-regulated, bax expression was up-regulated, mitochondrial membrane potential was significantly reduced, MPTP opened, cytc release from mitochondrion into cytoplasm was significantly increased, and both caspase-9 and caspase-3 activities were increased. Administration of an SO2 donor, however, markedly improved heart function and relieved myocardial injury of the ISO-treated rats; it lessened cardiomyocyte apoptosis, up-regulated myocardial bcl-2, down-regulated bax expression, stimulated mitochondrial membrane potential, closed MPTP, and reduced cytc release as well as caspase-9 and caspase-3 activities in the left ventricular tissue. Hence, SO2 attenuated myocardial injury in association with the inhibition of apoptosis in myocardial tissues, and the bcl-2/cytc/caspase-9/caspase-3 pathway was possibly involved in this process.
Keywords: isopropylarterenol; sulfur dioxide; myocardium; apoptosis; mitochondrial membrane potential
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MDPI and ACS Style
Jin, H.; Liu, A.D.; Holmberg, L.; Zhao, M.; Chen, S.; Yang, J.; Sun, Y.; Chen, S.; Tang, C.; Du, J. The Role of Sulfur Dioxide in the Regulation of Mitochondrion-Related Cardiomyocyte Apoptosis in Rats with Isopropylarterenol-Induced Myocardial Injury. Int. J. Mol. Sci. 2013, 14, 10465-10482.
Jin H, Liu AD, Holmberg L, Zhao M, Chen S, Yang J, Sun Y, Chen S, Tang C, Du J. The Role of Sulfur Dioxide in the Regulation of Mitochondrion-Related Cardiomyocyte Apoptosis in Rats with Isopropylarterenol-Induced Myocardial Injury. International Journal of Molecular Sciences. 2013; 14(5):10465-10482.
Jin, Hongfang; Liu, Angie D.; Holmberg, Lukas; Zhao, Manman; Chen, Siyao; Yang, Jinyan; Sun, Yan; Chen, Shanshan; Tang, Chaoshu; Du, Junbao. 2013. "The Role of Sulfur Dioxide in the Regulation of Mitochondrion-Related Cardiomyocyte Apoptosis in Rats with Isopropylarterenol-Induced Myocardial Injury." Int. J. Mol. Sci. 14, no. 5: 10465-10482.