Anti-apoptotic Potency of TNFR:Fc Gene in Ischemia/Reperfusion-Induced Myocardial Cell Injury

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• 作者：Jun Guo ; Dong Zheng ; Hai-Rui Li ; Ai-Dong Zhang ; Zi-Cheng Li
• 关键词：tumor necrosis factor ; apoptosis ; myocytes ; ischemia ; reperfusion ; hypoxia ; reoxygenation
• 刊名：Inflammation
• 出版年：2015
• 出版时间：April 2015
• 年：2015
• 卷：38
• 期：2
• 页码：664-671
• 全文大小：624 KB
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  3. Gurevitch, J, Frolkis, I, Yuhas, Y, Lifschitz Mercer, B, Berger, E, Paz, Y, Matsa, M, Kramer, A, Mohr, R (1997) Anti-tumor necrosis factor-alpha improves myocardial recovery after ischemia and reperfusion. Journal of the American College of Cardiology 30: pp. 1554-1561 CrossRef
  4. Bozkurt, B, Kribbs, SB, Clubb, FJ, Michael, LH, Didenko, VV, Hornsby, PJ, Seta, Y, Oral, H, Spinale, FG, Mann, DL (1998) Pathophysiologically relevant concentrations of tumor necrosis factor-α promote progressive left ventricular dysfunction and remodeling in rats. Circulation 97: pp. 1382-1391 CrossRef
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• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Rheumatology
  Internal Medicine
  Pharmacology and Toxicology
  Pathology
  
• 出版者：Springer Netherlands
• ISSN：1573-2576

文摘

The aim of the study was to investigate the anti-apoptotic potency of TNFR:Fc gene in ischemia/reperfusion-induced myocardial cell injury and hypoxia/reoxygenation-induced H9c2 rat cardiomyocytes injury. Rats were randomly divided into the following groups (n--): (1) sham operation group; (2) ischemia–reperfusion (I/R) rats treated with rAAV-EGFP; (3) I/R rats treated with rAAV-TNFR:Fc group. rAAV-EGFP or rAAV-TNFR:Fc was injected intra-myocardial at four sites on the anterior and posterior walls of left ventricle immediately after the construction of I/R-induced AMI model in rats. The effects of TNFR:Fc on apoptosis and cardiacfunction were observed after 72?h of coronary reperfusion. In the in vitro study, apoptosis was analyzed in H9c2 rat cardiomyocytes treated either with nomoxia alone, or hypoxia/reoxygenation in the presence of rAAV-GFP or rAAV-TNFR:Fc. We found that (1) TNFR:Fc gene improved cardiac function (EF, LVESP, LVEDP and dp/dt max) post I/R-induced AMI; (2) TNFR:Fc gene inhibited I/R-induced apoptosis and attenuated the level of TNF-α in serum and cardiac tissue; (3) TNFR:Fc gene prevented apoptosis in hypoxia/reoxygenation-induced H9c2 rat cardiomyocytes associated with inhibition of caspase-3 activation and normalization of ratio of the Bcl-2/Bax. We concluded that TNFR:Fc gene transfection has anti-apoptotic potency in ischemia/reperfusion-induced myocardial cell injury.