NDLI: Exogenous hydrogen sulfide attenuates diabetic myocardial injury through cardiac mitochondrial protection

Content Provider	Springer Nature Link
Author	Zhong, Xin Wang, Leihong Wang, Yuwen Dong, Shiyun Leng, Xiaoning Jia, Jing Zhao, Yajun Li, Hulun Zhang, Xinying Xu, Changqing Yang, Guangdong Wu, Lingyun Wang, Rui Lu, Fanghao Zhang, Weihua
Copyright Year	2012
Abstract	In the study, we investigated how exogenous H$_{2}$S (hydrogen sulfide) influenced streptozotocin (STZ)-induced diabetic myocardial injury through cardiac mitochondrial protection and nitric oxide (NO) synthesis in intact rat hearts and primary neonatal rat cardiomyocytes. Diabetes was induced by STZ (50 mg/kg) and the daily administration of 100 μM NaHS (sodium hydrosulfide, an H$_{2}$S donor) in the diabetes + NaHS treatment group. At the end of 4, 8, and 12 weeks, the morphological alterations and functions of the hearts were observed using transmission electron microscopy and echocardiography system. The percentage of apoptotic cardiomyocytes, the mitochondrial membrane potential, the production of reactive oxygen species (ROS) and the level of NO were measured. The expressions of cystathionine-γ-lyase (CSE), caspase-3 and -9, the mitochondrial NOX4 and cytochrome c were analyzed by western blotting. The results showed the cardiac function injured, morphological changes and the apoptotic rate increased in the diabetic rat hearts. In the primary neonatal rat cardiomyocytes of high glucose group, ROS production was increased markedly, whereas the expression of CSE and the level of NO was decreased. However, treatment with NaHS significantly reversed the diabetic rat hearts function, the morphological changes and decreased the levels of ROS and NO in the primary neonatal rat cardiomyocytes administrated with high glucose group. Furthermore, NaHS down-regulated the expression of mitochondrial NOX4 and caspase-3 and -9 and inhibited the release of cytochrome c from mitochondria in the primary neonatal rat cardiomyocytes. In conclusion, H$_{2}$S is involved in the attenuation of diabetic myocardial injury through the protection of cardiac mitochondria.
Starting Page	187
Ending Page	198
Page Count	12
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	371
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Springer US
Publisher Date	2012-09-23
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Hydrogen sulfide Diabetic myocardial injury Mitochondrial Nitric oxide Medical Biochemistry Cardiology Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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