caa a22 4500 606234179 CHVBK 20210128101236.0 cr unu---uuuuu 210128e20150101xx s 000 0 eng 10.1007/s11010-014-2245-6 doi (NATIONALLICENCE)springer-10.1007/s11010-014-2245-6 Sodium hydrosulfide attenuates hyperhomocysteinemia rat myocardial injury through cardiac mitochondrial protection [Elektronische Daten] [Yuwen Wang, Sa Shi, Shiyun Dong, Jichao Wu, Mowei Song, Xin Zhong, Yanhong Liu] Hydrogen sulfide (H2S) plays an important role during rat myocardial injury. However, little is known about the role of H2S in hyperhomocysteinemia (HHcy)-induced cardiac dysfunction as well as the underlying mechanisms. In this study, we investigated whether sodium hydrosulfide (NaHS, a H2S donor) influences methionine-induced HHcy rat myocardial injury in intact rat hearts and primary neonatal rat cardiomyocytes. HHcy rats were induced by methionine (2.0g/kg) and the daily administration of 80μmol/L NaHS in the HHcy+NaHS treatment group. At the end of 4, 8, and 12weeks, the ultrastructural alterations and functions of the hearts were observed using transmission electron microscopy and echocardiography system. The percentage of apoptotic cardiomyocytes, the mitochondrial membrane potential, and the production of reactive oxygen species (ROS) were measured. The expressions of cystathionine-γ-lyase (CSE), Bax and Bcl-2, caspase-3, phospho-endothelial nitric oxide synthase and the mitochondrial NOX4 and cytochrome c were analyzed by Western blotting. The results showed the cardiac dysfunction, the ultrastructural changes, and the apoptotic rate increase in the HHcy rat hearts. In the primary neonatal rat cardiomyocytes of HHcy group, ROS production was increased markedly, whereas the expression of CSE was decreased. However, treatment with NaHS significantly improved the HHcy rat hearts function, the ultrastructural changes, and decreased the levels of ROS in the primary neonatal rat cardiomyocytes administrated with HHcy group. Furthermore, NaHS down-regulated the expression of mitochondrial NOX4 and caspase-3 and Bax and inhibited the release of cytochrome c from mitochondria. In conclusion, H2S is involved in the attenuation of HHcy myocardial injury through the protection of cardiac mitochondria. Springer Science+Business Media New York, 2014 Sodium hydrosulfide nationallicence Hyperhomocysteinemia nationallicence Myocardial injury nationallicence Mitochondrial nationallicence Wang Yuwen Department of Clinical Laboratory, The Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, Heilongjiang, China aut Shi Sa Department of Pathophysiology, Harbin Medical University, 150086, Harbin, Heilongjiang, China aut Dong Shiyun Department of Pathophysiology, Harbin Medical University, 150086, Harbin, Heilongjiang, China aut Wu Jichao Department of Pathophysiology, Harbin Medical University, 150086, Harbin, Heilongjiang, China aut Song Mowei Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, 150001, Harbin, Heilongjiang, China aut Zhong Xin Department of Pathophysiology, Harbin Medical University, 150086, Harbin, Heilongjiang, China aut Liu Yanhong Department of Clinical Laboratory, The Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, Heilongjiang, China aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 399/1-2(2015-01-01), 189-200 0300-8177 399:1-2<189 2015 399 11010 https://doi.org/10.1007/s11010-014-2245-6 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-014-2245-6 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Wang Yuwen Department of Clinical Laboratory, The Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, Heilongjiang, China aut NATIONALLICENCE 700 1- Shi Sa Department of Pathophysiology, Harbin Medical University, 150086, Harbin, Heilongjiang, China aut NATIONALLICENCE 700 1- Dong Shiyun Department of Pathophysiology, Harbin Medical University, 150086, Harbin, Heilongjiang, China aut NATIONALLICENCE 700 1- Wu Jichao Department of Pathophysiology, Harbin Medical University, 150086, Harbin, Heilongjiang, China aut NATIONALLICENCE 700 1- Song Mowei Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, 150001, Harbin, Heilongjiang, China aut NATIONALLICENCE 700 1- Zhong Xin Department of Pathophysiology, Harbin Medical University, 150086, Harbin, Heilongjiang, China aut NATIONALLICENCE 700 1- Liu Yanhong Department of Clinical Laboratory, The Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, Heilongjiang, China aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 399/1-2(2015-01-01), 189-200 0300-8177 399:1-2<189 2015 399 11010