Effects of edaravone in heart of aged rats after cerebral ischemia-reperfusion injury

被引:8
|
作者
Watanabe, Kenichi
Ma, Meilei
Wen, Juan
Kodama, Makoto
Aizawa, Yoshifusa
机构
[1] Niigata Univ Pharm & Appl Life Sci, Dept Clin Pharmacol, Niigata 9568603, Japan
[2] Niigata Univ, Sch Med & Dent Sci, Dept Med 1, Niigata 9518510, Japan
关键词
edaravone; brain-to-heart signaling; cerebral ischemia reperfusion; oxidative stress; myocardial injury;
D O I
10.1248/bpb.30.460
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one) has potent effects in the brain as a free radical scavenger in ischemia-reperfusion (IR) injuries. However, whether this free radical scavenger can prevent myocardial injury after cerebral IR is not clear. The aim of the present study was to investigate the effect of edaravone against oxidative damage in brain-to-heart signaling triggered by IR injury and its possible mechanism. In this study, the expression of glutathione peroxidase (GSHPx) and protein carbonyl content was examined to evaluate oxidative stress. The activation of mitogen-activated protein kinases (MAPKs) was also examined. Terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) analysis was performed to estimate cardiomyocytes cell death. After edaravone treatment there was a mild increase in activities of GSHPx in cardiomyocytes; however, there was a decrease in protein carbonyl content. p38 MAPK activity was inhibited by edaravone treatment in comparison with the vehicle group in myocardium. These results were further complemented by a significant reduction of TUNEL-positive cells in the heart sections. Our results demonstrate that edaravone provides ameliorative effects in the myocardium after cerebral IR injury by differentially modulating MAPK's activity, thus reducing the oxidative stress state.
引用
收藏
页码:460 / 464
页数:5
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