NDLI: GYY4137, a hydrogen sulfidereleasing molecule, inhibits the inflammatory response by suppressing the activation of nuclear factorkappa B and mitogenactivated protein kinases in Coxsackie virus B3infected rat cardiomyocytes.

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GYY4137, a hydrogen sulfidereleasing molecule, inhibits the inflammatory response by suppressing the activation of nuclear factorkappa B and mitogenactivated protein kinases in Coxsackie virus B3infected rat cardiomyocytes.

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GYY4137, a hydrogen sulfidereleasing molecule, inhibits the inflammatory response by suppressing the activation of nuclear factorkappa B and mitogenactivated protein kinases in Coxsackie virus B3infected rat cardiomyocytes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wu, Zubo Du, Qing Lin, Wen Liu, Yali Peng, Hua
Description	Author Affiliation: Wu Z ( Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.); Peng H ( Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.); Du Q ( Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.); Lin W ( Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.); Liu Y ( Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.)
Abstract	GYY4137 is a watersoluble, small molecule hydrogen sulfide (H2S)release agent that possesses potent cardioprotective and antiinflammatory properties in experimental models. Coxsackie virus B3 (CVB3) infection commonly causes viral myocarditis, which mainly involves immune cell infiltration, eventually resulting in heart failure. In the present study, the effects and underlying mechanisms of GYY4137 treatment of CVB3induced myocarditis were investigated. The effects of GYY4137 on CVB3induced nuclear factorkappa B (NFκB) activity were examined by western blotting, immunofluorescence and electrophoretic mobility shift assay. Mitogenactivated protein kinase (MAPK) signaling protein expression levels were detected by western blotting. Cardiomyocyte damagerelated enzyme activities, such as lactate dehydrogenase (LDH) and creatine kinase MB (CKMB), were measured by ELISA, as well as the production of proinflammatory cytokines. The results revealed that GYY4137 suppressed CVB3induced secretion of LDH, CKMB and proinflammatory cytokines, such as tumor necrosis factor , interleukin (IL)1ß and IL6. Furthermore, the activation of NFκB and the IκB degradation induced by CVB3 were also inhibited by GYY4137. Notably, the phosphorylation of p38, ERK1/2 and JNK1/2 induced by CVB3 was also inhibited by GYY4137. In conclusion, the data demonstrate that GYY4137 exerts antiinflammatory effects in CVB3infected cardiomyocytes. This antiinflammatory mechanism may be associated with suppression of NFκB and MAPK signaling pathway activation.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-03-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Anti-inflammatory Agents Pharmacology Enterovirus B, Human Physiology Mitogen-activated Protein Kinases Metabolism Morpholines Myocytes, Cardiac Virology Nf-kappa B Organothiophosphorus Compounds Active Transport, Cell Nucleus Animals Administration & Dosage Cells, Cultured Coxsackievirus Infections Complications Dna-binding Proteins Enzyme Activation Drug Effects Hydrogen Sulfide Inflammation Mediators Myocarditis Drug Therapy Etiology Protein Transport Proteolysis Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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