NDLI: Nitric oxide synthase inhibition abrogates hydrogen sulfide-induced cardioprotection in mice

Content Provider	Springer Nature Link
Author	Sojitra, Bhavesh Bulani, Yogesh Putcha, Uday Kumar Kanwal, Abhinav Gupta, Prachi Kuncha, Madhusudana Banerjee, Sanjay Kumar
Copyright Year	2011
Abstract	The cardioprotective property of hydrogen sulfide (H$_{2}$S) is recently reported. However, cellular signaling cascades mediated by H$_{2}$S are largely unclear. This study was undertaken to explore the molecular mechanism of H$_{2}$S-induced cardioprotection in mouse heart by utilizing in vivo model of cardiac injury. We report here that intraperitoneal administration of sodium hydrogen sulfide (NaHS, 50 μmol kg$^{−1 }$day$^{−1}$ for 2 days), a H$_{2}$S donor, significantly (P ≤ 0.05) increased nitric oxide levels in serum as well as myocardium without any sign of myocardial injury. Typical characteristics of myocardial injury induced by isoproterenol (ISO) administration was significantly (P ≤ 0.05) abrogated by NaHS administration as evidenced from reduction in elevated thiobarbituric acid reactive substances (TBARS) and normalization of glutathione (GSH), glutathione peroxidase, superoxide dismutase (SOD), and catalase activity. Further, decrease in TNF-α expression and improvement in myocardial architecture was also observed. However, co-administration of N-nitro-l-arginine methyl ester, a nitric oxide synthase (NOS) inhibitor, and Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor along with NaHS and ISO abrogated the beneficial effect of H$_{2}$S differentially. Inhibition of NOS significantly (P ≤ 0.05) increased serum creatine kinase, lactate dehydrogenase, serum glutamic oxaloacetic transaminase activity and myocardial TBARS, along with significant (P ≤ 0.05) reduction of myocardial GSH, SOD, and catalase. This was followed by increase in TNF-α expression and histopathological changes. Our results revealed that H$_{2}$S provides myocardial protection through interaction with NOS and COX-2 pathway and inhibition of NOS completely abrogates the hydrogen sulfide-induced cardioprotection in mice.
Starting Page	61
Ending Page	69
Page Count	9
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	360
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Springer US
Publisher Date	2011-08-31
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Hydrogen sulfide Isoproterenol Cardioprotection Cyclooxygenase-2 Nitric oxide Medical Biochemistry Oncology Cardiology 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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