Hydrogen sulfide preconditioning protects against myocardial ischemia/reperfusion injury in rats through inhibition of endo/sarcoplasmic reticulum stress.
Ischemia reperfusion (I/R) injury is a major cause of myocardial damage. Hydrogen sulfide (H2S), a gaseous signal molecule, has drawn considerable attention for its role in various pathophysiological processes. Multiple lines of evidence reveal the protective effects of H2S in various models of cardiac injury, however, the exact mechanism underlying this protective effect of H2S against myocardial I/R injury is not fully understood. The present study was designed to investigate whether H2S preconditioning attenuates myocardial I/R injury in rats and whether the observed protection is associated with reduced endo/sarcoplasmic reticulum (ER/SR) stress. We found that H2S preconditioning significantly reduced myocardial infarct size, preserved left ventricular function, and inhibited I/R-induced cardiomyocyte apoptosis in vivo. Furthermore, H2S preconditioning significantly attenuated I/R-induced ER/SR stress responses, including the increased expression of glucose-regulated protein 78, C/EBP homologous protein, and activate transcription factor in myocardium. Additionally, we demonstrate that H2S preconditioning attenuates ER/SR stress and inhibits cardiomyocyte apoptosis in an in vitro model of hypoxia/reoxygenation in rat H9c2 cardiac myocytes. In conclusion, these results suggest that H2S-attenuated ER/SR stress plays an important role in its protective effects against I/R-induced myocardial injury.
Department of Physiology, School of Basic Medical Sciences, Wuhan University Wuhan, Hubei, China.
Changyong
C
Li
Department of Physiology, School of Basic Medical Sciences, Wuhan University Wuhan, Hubei, China.
Min
M
Hu
Department of Physiology, School of Basic Medical Sciences, Wuhan University Wuhan, Hubei, China.
Yuan
Y
Wang
Department of Physiology, School of Basic Medical Sciences, Wuhan University Wuhan, Hubei, China.
Huan
H
Lu
Department of Physiology, School of Basic Medical Sciences, Wuhan University Wuhan, Hubei, China.
Jing
J
Deng
Department of Physiology, School of Basic Medical Sciences, Wuhan University Wuhan, Hubei, China.
Xiaohong
X
Yan
D000818:Animals; D017209:Apoptosis; D005786:Gene Expression Regulation; D018840:HSP70 Heat-Shock Proteins / Q000235:genetics; D006801:Humans; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D009203:Myocardial Infarction / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000502:physiology; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D012519:Sarcoplasmic Reticulum / Q000502:physiology
D018840:HSP70 Heat-Shock Proteins; D008565:Membrane Proteins; D020011:Protective Agents; C018551:glucose-regulated proteins; D006862:Hydrogen Sulfide
Ischemia/reperfusion; endo/sarcoplasmic reticulum stress; hydrogen sulfide; myocardial protection