Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model

被引:9
作者
Gonzalez-Pacheco, Hector [1 ,2 ]
Mendez-Dominguez, Aurelio [3 ]
Hernandez, Salomon [4 ]
Lopez-Marure, Rebeca [5 ]
Vazquez-Mellado, Maria J. [6 ]
Aguilar, Cecilia [6 ]
Rocha-Zavaleta, Leticia [6 ]
机构
[1] Inst Nacl Cardiol Ignacio Chavez, Dept Urgencias, Tlalpan 14080, DF, Mexico
[2] Inst Nacl Cardiol Ignacio Chavez, Unidad Coronaria, Tlalpan 14080, DF, Mexico
[3] Inst Nacl Cardiol Ignacio Chavez, Dept Neurol, Tlalpan 14080, DF, Mexico
[4] Univ Panamericana, Fac Med, Insurgentes Mixcoac 03920, DF, Mexico
[5] Inst Nacl Cardiol Ignacio Chavez, Dept Biol Celular, Tlalpan 14080, DF, Mexico
[6] UNAM, Inst Invest Biomed, Dept Mol Biol & Biotechnol, Circuito Escolar S-N,Ciudad Univ, Coyoacan 04510, DE, Mexico
关键词
FREE-RADICALS; REPERFUSION; LYSOPHOSPHATIDYLCHOLINE; ISCHEMIA; CELLS; METABOLISM; APOPTOSIS; OXIDANTS; STROKE;
D O I
10.1155/2014/187071
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background. CDP-choline is a key intermediate in the biosynthesis of phosphatidylcholine, which is an essential component of cellular membranes, and a cell signalling mediator. CDP-choline has been used for the treatment of cerebral ischaemia, showing beneficial effects. However, its potential benefit for the treatment of myocardial ischaemia has not been explored yet. Aim. In the present work, we aimed to evaluate the potential use of CDP-choline as a cardioprotector in an in vitro model of ischaemia/reperfusion injury. Methods. Neonatal rat cardiac myocytes were isolated and subjected to hypoxia/reperfusion using the coverslip hypoxia model. To evaluate the effect of CDP-choline on oxidative stress-induced reperfusion injury, the cells were incubated with H2O2 during reperfusion. The effect of CDP-choline pre- and postconditioning was evaluated using the cell viability MTT assay, and the proportion of apoptotic and necrotic cells was analyzed using the Annexin V determination by flow cytometry. Results. Pre- and postconditioning with 50 mg/mL of CDP-choline induced a significant reduction of cells undergoing apoptosis after hypoxia/reperfusion. Preconditioning with CDP-choline attenuated postreperfusion cell death induced by oxidative stress. Conclusion. CDP-choline administration reduces cell apoptosis induced by oxidative stress after hypoxia/reperfusion of cardiac myocytes. Thus, it has a potential as cardioprotector in ischaemia/reperfusion-injured cardiomyocytes.
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页数:8
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共 28 条
[1]   Cytidine 5′-diphosphocholine (CDP-choline) in stroke and other CNS disorders [J].
Adibhatla, R ;
Hatcher, JF .
NEUROCHEMICAL RESEARCH, 2005, 30 (01) :15-23
[2]   Cytidine-5'-diphosphocholine affects CTP-phosphocholine cytidylyltransferase and lyso-phosphatidylcholine after transient brain ischemia [J].
Adibhatla, RM ;
Hatcher, JF ;
Dempsey, RJ .
JOURNAL OF NEUROSCIENCE RESEARCH, 2004, 76 (03) :390-396
[3]   How and When Do Myocytes Die During Ischemia and Reperfusion: The Late Phase [J].
Baines, Christopher P. .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY AND THERAPEUTICS, 2011, 16 (3-4) :239-243
[4]   DIRECT EVIDENCE THAT OXYGEN-DERIVED FREE-RADICALS CONTRIBUTE TO POSTISCHEMIC MYOCARDIAL DYSFUNCTION IN THE INTACT DOG [J].
BOLLI, R ;
JEROUDI, MO ;
PATEL, BS ;
DUBOSE, CM ;
LAI, EK ;
ROBERTS, R ;
MCCAY, PB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (12) :4695-4699
[5]   EFFICACY AND SAFETY OF ORAL CITICOLINE IN ACUTE ISCHEMIC STROKE: DRUG SURVEILLANCE STUDY IN 4,191 CASES [J].
Cho, H. -J. ;
Kim, Y. J. .
METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY, 2009, 31 (03) :171-176
[6]   PHOSPHATIDYLCHOLINE METABOLISM IN ISCHEMIC AND HYPOXIC HEARTS [J].
CHOY, PC ;
CHAN, M ;
HATCH, G ;
MAN, RYK .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 1992, 116 (1-2) :53-58
[7]   PHOSPHATIDYLCHOLINE BREAKDOWN AND SIGNAL-TRANSDUCTION [J].
EXTON, JH .
BIOCHIMICA ET BIOPHYSICA ACTA-LIPIDS AND LIPID METABOLISM, 1994, 1212 (01) :26-42
[8]   DIRECT MEASUREMENT OF MYOCARDIAL FREE-RADICAL GENERATION IN AN INVIVO MODEL - EFFECTS OF POSTISCHEMIC REPERFUSION AND TREATMENT WITH HUMAN RECOMBINANT SUPEROXIDE-DISMUTASE [J].
GRILL, HP ;
ZWEIER, JL ;
KUPPUSAMY, P ;
WEISFELDT, ML ;
FLAHERTY, JT .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1992, 20 (07) :1604-1611
[9]   TNF provokes cardiomyocyte apoptosis and cardiac remodeling through activation of multiple cell death pathways [J].
Haudek, Sandra B. ;
Taffet, George E. ;
Schneider, Michael D. ;
Mann, Douglas L. .
JOURNAL OF CLINICAL INVESTIGATION, 2007, 117 (09) :2692-2701
[10]   Lysophosphatidylcholine induces apoptotic and non-apoptotic death in vascular smooth muscle cells: in comparison with oxidized LDL [J].
Hsieh, CC ;
Yen, MH ;
Liu, HW ;
Lau, YT .
ATHEROSCLEROSIS, 2000, 151 (02) :481-491