Effect of edaravone on the apoptosis and expression of Cuspase-3 protein following focal cerebral ischemia/reperfusion injury in rats
10.3760/cma.j.issn.1671-8925.2008.10.010
- VernacularTitle:依达拉奉对大鼠局灶性脑缺血再灌注损伤后细胞凋亡及caspase-3蛋白表达的影响
- Author:
Hui-Fang XIE
1
;
Ru-Xiang XU
;
Ji-Peng WEI
;
Xiao-Dan JIANG
;
Zhen-Hua LIU
;
Mou-Xuan DU
Author Information
1. 南方医科大学珠江医院
- Keywords:
Cerebral ischemia/reperfusion;
Edatavone;
Caspase-3;
Apoptosis
- From:
Chinese Journal of Neuromedicine
2008;7(10):1009-1012
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of edaravone (ED) on the neurological functionaldeficits, apoptosis and expression of caspase-3 protein following focal cerebral ischemia/reperfusion(I/R)injury in rats. Methods A total of 24 male Sprague-Dawley (SD) rats were randomly allocated intothe sham-operation group, cerebral I/R group, normal saline treatment group and ED treatment group, 6rats in each group. Rat models with focal cerebral I/R injury induced by middle cerebral artery occlusion(MCAO) were established using a modified suture method. ED (3mg/kg) or equal volume of normalsaline was injected intraperitoneally immediately after cerebral ischemia and 12 h after reperfusion in thetreatment groups;the rats in sham-operation group underwent the same modeling procedure withoutischemia by nylon suture. The neurological behavioral deficits were evaluated 24 h after I/R injury;,immunohistochemical staining and Western blot assay were applied to detect the change in the expressionof caspase-3 protein; in situ TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay was used tostudy the change in neuronal apoptosis. Results The scores of neurological behavioral deficit scale,the positive cells and expression of caspase-3 protein, and the apoptotic cells in the ED treatment groupwere significantly decreased, compared with that of the I/R group and normal saline treatment group(P<0.05 for each comparison). Conclusion ED may effectively reduce neuronal apuptosis andneurological functional deficits after cerebral I/R injury, which might be related with the inhibition of thecaspase-3 protein expression.
