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Soluble form of the receptor for advanced glycation end products inhibits cardiac dysfunction and myocardial apoptosis induced by ischemia-reperfusion
GUO Cai-xia* JIANG Xue ZENG Xiang-jun WANG Hong-xia DU Feng-he CHEN Bu-xing*
Acta Anatomica Sinica ›› 2015, Vol. 46 ›› Issue (2) : 202-207.
Soluble form of the receptor for advanced glycation end products inhibits cardiac dysfunction and myocardial apoptosis induced by ischemia-reperfusion
Objective To test the effect of sRAGE on cardiac function and myocardial apoptosis induced by ischemia-reperfusion in vivo. Methods C57BL/6J mice with the ligation of left anterior descending coronary artery were used as the in vivomodel. At the end of reperfusion, cardiac function was evaluated with echocardiography, and myocardial apoptosis was detected by TUNEL staining and caspase-3 activaty. Results Compared to the sham group, I/R decreased left ventricular ejection fractions (EF)［(30.9±3.2)% vs (72.4±2.1)%，P<0.05］, and left ventricular fractional shortening (FS)［(15.1±2.0)% vs( 40.7±1.6)%, P<0.05］, and then increased TUNEL ［(20.0±1.6)% vs(1.0±0.2)%,P<0.05］, and Caspase-3 activaty ［(2.64±0.4)% vs(1.00±0.2)%, P<0.05］. Compared to I/R group, sRAGE pretreatment significantly improved EF ［(46.5±2.0)% vs (30.9±3.2)%, P<0.05］, and FS［ (23.0±1.1)%vs (15.1±2.0)%, P<0.05］, decreased TUNEL ［(9.2±1.0)% vs (20.0±1.6)%,P<0.05］, and Caspase-3 activaty［ (1.94±0.1)% vs (2.64±0.4)% ,P<0.05］. Conclusion sRAGE inhibits cardiac dysfunction and myocardial apoptosis induced by ischemia-reperfusion in vivo.
Soluble form of receptor for advanced glycation end product / Ischemia-reperfusion / Cardiac function / Myocardium / Terminal UTP nick end labeling / Mouse
［1］Ma HJ, Li Q, Ma HJ, et al., Chronic intermittent hypobaric hypoxia ameliorates ischemia/reperfusion-induced calcium overload in heart via Na/Ca2+ exchanger in developing rats［J］. Cell Physiol Biochem, 2014, 34(2): 313-324.
［2］Matsushima S, Tsutsui H, Sadoshima J. Physiological and pathological functions of NADPH oxidases during myocardial ischemia-reperfusion［J］. Trends Cardiovasc Med, 2014, 24(5): 202-205.
［3］Braunersreuther V, Montecucco F, Asrih M, et al. Role of NADPH oxidase isoforms NOX1, NOX2 and NOX4 in myocardial ischemia/reperfusion injury［J］. J Mol Cell Cardiol, 2013, 64: 99-107.
［4］Cash JL, Bena S, Headland SE, et al., Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury through ChemR23［J］. EMBO Rep, 2013, 14(11): 999-1007.
［5］Orogo AM, Gustafsson B. Cell death in the myocardium: my heart won’t go on［J］. IUBMB Life, 2013, 65(8): 651-656.
［6］Shang L, Ananthakrishnan R, Li Q, et al. RAGE modulates hypoxia/reoxygenation injury in adult murine cardiomyocytes via JNK and GSK3beta signaling pathways［J］. PLoS One, 2010, 5(4): e10092.
［7］Basta G. Receptor for advanced glycation endproducts and atherosclerosis: from basic mechanisms to clinical implications［J］. Atherosclerosis, 2008, 196(1): 9-21.
［8］Yan SF, Ramasamy R, Schmidt AM. Soluble RAGE: therapy and biomarker in unraveling the RAGE axis in chronic disease and aging［J］. Biochem Pharmacol, 2010, 79(10): 1379-1386.
［9］Guo C, Zeng X, Song J, et al. A Soluble receptor for advanced glycation end-products inhibits hypoxia/reoxygenation-induced apoptosis in rat cardiomyocytes via the mitochondrial pathway［J］. Int J Mol Sci, 2012,13(9): 11923-11940.
［10］Pan Z, Sun X, Ren J, et al. miR-1 exacerbates cardiac ischemia-reperfusion injury in mouse models［J］. PLoS One, 2012, 7(11): e50515.
［11］Toldo S, Seropian IM, Mezzaroma E, et al. Alpha-1 antitrypsin inhibits caspase-1 and protects from acute myocardial ischemia-reperfusion injury［J］. J Mol Cell Cardiol, 2011, 51(2): 244-251.
［12］Yin T, Hou R, Liu S, et al. Nitrative inactivation of thioredoxin-1 increases vulnerability of diabetic hearts to ischemia/reperfusion injury［J］. J Mol Cell Cardiol, 2010, 49(3): 354-361.
［13］Wang K, Zhang J, Liu J, et al. Variations in the protein level of Omi/HtrA2 in the heart of aged rats may contribute to the increased susceptibility of cardiomyocytes to ischemia/reperfusion injury and cell death : Omi/HtrA2 and aged heart injury［J］. Age (Dordr), 2013,35(3): 733-746.
［14］Qian W, Xiong X, Fang Z, et al. Protective effect of tetramethylpyrazine on myocardial ischemia-reperfusion injury［J］. Evid Based Complement Alternat Med, 2014,2014: 107501.
［15］Badalzadeh R, Yousefi B, Majidinia M, et al. Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial K channel［J］. J Physiol Sci, 2014,64(6):393-400
［16］Rosano GM, Fini M, Caminiti G, et al. Cardiac metabolism in myocardial ischemia［J］. Curr Pharm Des, 2008,14(25): 2551-2562.
［17］Wu F, Feng JZ, Qiu YH, et al. Activation of receptor for advanced glycation end products contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated rats［J］. Atherosclerosis, 2013, 229(2): 287-294.
［18］Tsoporis JN, Izhar S, Leong-Poi H, et al. S100B interaction with the receptor for advanced glycation end products (RAGE): a novel receptor-mediated mechanism for myocyte apoptosis postinfarction［J］. Circ Res, 2010, 106(1): 93-101.
［19］Bucciarelli LG, Kaneko M, Ananthakrishnan R, et al. Receptor for advanced-glycation end products: key modulator of myocardial ischemic injury［J］. Circulation, 2006,113(9): 1226-1234.
［20］Fliss H, Gattinger D. Apoptosis in ischemic and reperfused rat myocardium［J］. Circ Res, 1996, 79(5): 949-956.
［21］Koyama H, Tanaka S, Monden M, et al. Comparison of effects of pioglitazone and glimepiride on plasma soluble RAGE and RAGE expression in peripheral mononuclear cells in type 2 diabetes: randomized controlled trial (PioRAGE) ［J］. Atherosclerosis, 2014, 234(2): 329-334.
［22］Metz VV, Kojro E, Rat D, et al. Induction of RAGE shedding by activation of G protein-coupled receptors［J］. PLoS One, 2012, 7(7): e41823.
［23］Yan SF, Ramasamy R, Schmidt AM. The receptor for advanced glycation endproducts (RAGE) and cardiovascular disease［J］. Expert Rev Mol Med, 2009, 11: e9.
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