Preconditioning with diosgenin and treadmill exercise preserves the cardiac toxicity of isoproterenol in rats

被引:20
作者
Salimeh, Afshin [1 ]
Mohammadi, Mustafa [1 ]
Rashidi, Bahman [2 ]
机构
[1] Tabriz Univ Med Sci, Drug Appl Res Ctr, Dept Physiol, Tabriz, Iran
[2] Isfahan Univ Med Sci, Sch Med, Dept Anat & Histol, Esfahan, Iran
关键词
Myocardial infarction; Diosgenin; Exercise; Lipid peroxidation; Antioxidant enzymes; EXPERIMENTAL MYOCARDIAL-INFARCTION; CHRONIC HEART-FAILURE; OXIDATIVE STRESS; ISCHEMIA-REPERFUSION; LIPID-PEROXIDATION; GLUTATHIONE; FLOW; ATHEROSCLEROSIS; MITOCHONDRIAL; EXPRESSION;
D O I
10.1007/s13105-012-0208-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study was aimed to evaluate the preventive effect of diosgenin and exercise on tissue antioxidant status in isoproterenol-induced myocardial infarction (MI) in male Wistar rats. Levels of lipid peroxides, reduced glutathione (GSH), and the activities of glutathione-dependent antioxidant enzymes (glutathione peroxidise and glutathione reductase) and antiperoxidative enzymes (catalase and superoxide dismutase) in the plasma and the heart tissue of experimental groups of rats were determined. Pretreatment with diosgenin and exercise exerted an antioxidant effect against isoproterenol-induced myocardial infarction by blocking the induction of lipid peroxidation. A tendency to prevent the isoproterenol-induced alterations in the level of GSH, in the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes was also observed. Histopathological findings of the myocardial tissue showed a protective role for combination of diosgenin and exercise in isoproterenol (ISO)-treated rats. Thus, the present study reveals that preconditioning with diosgenin and exercise exerts cardioprotective effect against ISO-induced MI due to its free radical scavenging and antioxidant effects, which maintains the tissue defense system against myocardial damage.
引用
收藏
页码:255 / 265
页数:11
相关论文
共 62 条
[1]  
AEBI H, 1984, METHOD ENZYMOL, V105, P121
[2]   Oxidative stress and gene regulation [J].
Allen, RG ;
Tresini, M .
FREE RADICAL BIOLOGY AND MEDICINE, 2000, 28 (03) :463-499
[3]  
Anandan R, 1999, CURR SCI INDIA, V76, P1543
[4]  
Anandan R, 2003, J CLIN BIOCHEM NUTR, V25, P87
[5]   Modulation of antioxidant enzymes and lipid peroxidation in salivary gland and other tissues in mice by moderate treadmill exercise [J].
Avula, CPR ;
Fernandes, G .
AGING CLINICAL AND EXPERIMENTAL RESEARCH, 1999, 11 (04) :246-252
[6]   Mortality attributable to cardiovascular risk factors in Spain [J].
Banegas, JR ;
Rodríguez-Artalejo, F ;
Graciani, A ;
Villar, F ;
Herruzo, R .
EUROPEAN JOURNAL OF CLINICAL NUTRITION, 2003, 57 (Suppl 1) :S18-S21
[7]   MYOCARDIAL NECROSIS - NEED FOR DEFINITION [J].
BAROLDI, G .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1974, 6 (04) :401-+
[8]   Comparing Effects of Lacidipine, Ramipril, and Valsartan Against Experimentally Induced Myocardial Infarcted Rats [J].
Bayir, Yasin ;
Halici, Zekai ;
Karakus, Emre ;
Albayrak, Abdulmecit ;
Ferah, Irmak ;
Kabalar, Esref ;
Keles, Osman ;
Keles, Mevlut Sait ;
Unal, Bunyami .
CARDIOVASCULAR TOXICOLOGY, 2012, 12 (02) :166-174
[9]   Diabetes and atherosclerosis - Epidemiology, pathophysiology, and management [J].
Beckman, JA ;
Creager, MA ;
Libby, P .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2002, 287 (19) :2570-2581
[10]   THE STUNNED MYOCARDIUM - PROLONGED, POST-ISCHEMIC VENTRICULAR DYSFUNCTION [J].
BRAUNWALD, E ;
KLONER, RA .
CIRCULATION, 1982, 66 (06) :1146-1149