Mitochondrial ATP-sensitive K+ channels mediate the antioxidative influence of diosgenin on myocardial reperfusion injury in rat hearts

被引：23
作者：
Badalzadeh, Reza [1 ,2 ,3 ]
Yavari, Raana [3 ]
Chalabiani, Dorna [3 ]
机构：
[1] Tabriz Univ Med Sci, Drug Appl Res Ctr, Tabriz, Iran
[2] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran
[3] Tabriz Univ Med Sci, Dept Physiol, Fac Med, Tabriz, Iran
来源：
GENERAL PHYSIOLOGY AND BIOPHYSICS | 2015年 / 34卷 / 03期
关键词：
Diosgenin; Oxidative stress; Mito K-ATP channels; I/R injury; POTASSIUM CHANNELS; NITRIC-OXIDE; DIOSCOREA; GENERATION; INCREASES; RELEASE; SAPONIN; SYSTEM; YAM;
D O I：
10.4149/gpb_2015009
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：
The contribution of reactive oxygen species and oxidative stress in the pathogenesis of ischemia-reperfusion (I/R) injury has been supported by many studies. The effect of diosgenin on oxidative stress induced by I/R injury was evaluated in this study. Rat hearts were subjected to 30 minutes of global ischemia followed by 90 minutes of reperfusion. 5-hydroxydecanoate (5-HD) was used before administration of diosgenin and before ischemia. The activities of myocardial creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were measured. Administration of diosgenin before ischemia significantly lowered CK and MDA levels as compared with control group (p < 0.05) and increased GPX (p < 0.05) and SOD (p < 0.01) activities in comparison with control group. Pre-administration of 5-HD significantly attenuated the protective effects of diosgenin. In conclusion, opening of mitochondrial ATP-sensitive K+ channels and attenuating of oxidative stress can be suggested as underlying mechanisms for cardioprotective effect of diosgenin in I/R injury.
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收藏
页码：323 / 329
页数：7
相关论文
共 31 条
[1]   Opening of mitochondrial K+ channels increases ischemic ATP levels by preventing hydrolysis [J].
Belisle, E ;
Kowaltowski, AJ .
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, 2002, 34 (04) :285-298
[2]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[3]   MYOCARDIAL REPERFUSION - A DOUBLE-EDGED SWORD [J].
BRAUNWALD, E ;
KLONER, RA .
JOURNAL OF CLINICAL INVESTIGATION, 1985, 76 (05) :1713-1719
[4]   Protective effects of diosgenin in the hyperlipidemic rat model and in human vascular endothelial cells against hydrogen peroxide-induced apoptosis [J].
Cong, Guohua ;
Qin, Yuan ;
Huang, Wen ;
Zhou, Shu ;
Wu, Xiaohua ;
Yang, Xiaohua ;
Zhao, Yinlan ;
Li, Dan .
CHEMICO-BIOLOGICAL INTERACTIONS, 2010, 184 (03) :366-375
[5]  
Corbiere C, 2003, INT J ONCOL, V22, P899
[6]   RELATIONSHIP BETWEEN RED-BLOOD-CELL ANTIOXIDANT ENZYMATIC SYSTEM STATUS AND LIPOPEROXIDATION DURING THE ACUTE-PHASE OF MALARIA [J].
DELMASBEAUVIEUX, MC ;
PEUCHANT, E ;
DUMON, MF ;
RECEVEUR, MC ;
LEBRAS, M ;
CLERC, M .
CLINICAL BIOCHEMISTRY, 1995, 28 (02) :163-169
[7]  
DRAPER HH, 1990, METHOD ENZYMOL, V186, P421
[8]   Diosgenin attenuates inflammatory response induced by myocardial reperfusion injury: role of mitochondrial ATP-sensitive potassium channels [J].
Ebrahimi, Hadi ;
Badalzadeh, Reza ;
Mohammadi, Mustafa ;
Yousefi, Bahman .
JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY, 2014, 70 (02) :425-432
[9]   Mitochondrial ATP-sensitive K+ channels are redox-sensitive pathways that control reactive oxygen species production [J].
Facundo, Heberty T. F. ;
de Paula, Juliana G. ;
Kowaltowski, Alicia J. .
FREE RADICAL BIOLOGY AND MEDICINE, 2007, 42 (07) :1039-1048
[10]   Ischemic preconditioning requires increases in reactive oxygen release independent of mitochondrial K+ channel activity [J].
Facundo, HTF ;
Carreira, RS ;
de Paula, JG ;
Santos, CCX ;
Ferranti, R ;
Laurindo, FRM ;
Kowaltowski, AJ .
FREE RADICAL BIOLOGY AND MEDICINE, 2006, 40 (03) :469-479
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