CAJ | 학술논문

目的探讨依达拉奉对大鼠局灶性脑缺血再灌注损伤后神经功能损伤、细胞凋亡及caspasc-3蛋白表达的影响.方法雄性SD大鼠24只采用随机数字表法分为假手术组、脑缺血再灌注组、生理盐水治疗组、依达拉奉治疗组,每组6只.除假手术组外,其余3组均采用大脑中动脉线栓法制作大鼠局灶性脑缺血再灌注损伤模型.依达拉奉治疗组于脑缺血开始时及再灌注后12 h分别腹腔注射依达拉奉3 mg/kg,生理盐水治疗组同时间注射等量生理盐水;假手术组同样过程造模,但不插入尼龙线造成缺血.造模后24 h后进行大鼠神经行为学评分;应用免疫组织化学及Western blot检测caspase-3蛋白表达水平的变化;利用原位缺口末端标记法(TUNEL法)研究神经细胞凋亡的变化.结果与脑缺血再灌注组及生理盐水治疗组相比,依达拉奉治疗组大鼠神经行为学评分明显减少,caspase-3免疫阳性细胞及蛋白表达明显减少,凋亡细胞也减少,差异均有统计学意义(P<0.05).结论依达拉奉能有效减轻脑缺血灌注损伤后神经细胞凋亡.改善神经功能缺损症状,推测其机制与抑制caspase-3蛋白表达有关.
목적 탐토의체랍봉대대서국조성뇌결혈재관주손상후신경공능손상、세포조망급caspasc-3단백표체적영향.방법 웅성SD대서24지채용수궤수자표법분위가수술조、뇌결혈재관주조、생리염수치료조、의체랍봉치료조,매조6지.제가수술조외,기여3조균채용대뇌중동맥선전법제작대서국조성뇌결혈재관주손상모형.의체랍봉치료조우뇌결혈개시시급재관주후12 h분별복강주사의체랍봉3 mg/kg,생리염수치료조동시간주사등량생리염수;가수술조동양과정조모,단불삽입니룡선조성결혈.조모후24 h후진행대서신경행위학평분;응용면역조직화학급Western blot검측caspase-3단백표체수평적변화;이용원위결구말단표기법(TUNEL법)연구신경세포조망적변화.결과 여뇌결혈재관주조급생리염수치료조상비,의체랍봉치료조대서신경행위학평분명현감소,caspase-3면역양성세포급단백표체명현감소,조망세포야감소,차이균유통계학의의(P<0.05).결론 의체랍봉능유효감경뇌결혈관주손상후신경세포조망.개선신경공능결손증상,추측기궤제여억제caspase-3단백표체유관.
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.