CAJ | 학술논문

目的明确银丹心脑通对脑缺血再灌注时神经细胞凋亡的保护作用,探索其治疗缺血性脑卒中的分子作用机制. 方法将40只SD雄性大鼠按随机数字表法分为假手术组、模型组、阳性对照组(尼莫地平组)、银丹心脑通组.尼莫地平组及银丹心脑通组预先连续灌胃给药7d,假手术组和模型组每日灌服相当量的蒸馏水,第8大制备大鼠大脑中动脉阻塞模型.脑缺血再灌注24 h后应用TUNEL法检测各组大鼠海马CA1区凋亡阳性神经细胞数,应用免疫组化染色测定各组大鼠脑组织中天冬氨酸特异性半胱氨酸蛋白酶-3(Caspase-3)的表达. 结果模型组大鼠均能见到较多的凋亡阳性细胞数及Caspase-3阳性细胞数,与假手术组比较差异有统计学意义(P＜0.05)；与模型组比较,银丹心脑通组、尼莫地平组能明显减小凋亡阳性细胞数及Caspase-3阳性细胞数,差异有统计学意义(P＜0.05)；银丹心脑通组与尼莫地平组在凋亡阳性神经细胞数及Caspase-3阳性细胞数上比较差异无统计学意义(P＞0.05). 结论银丹心脑通对脑缺血再灌注损伤有一定保护作用,能够减少脑缺血再灌注大鼠神经细胞的凋亡,其作用机制可能与减少脑组织中Caspase-3的表达有关.
목적 명학은단심뇌통대뇌결혈재관주시신경세포조망적보호작용,탐색기치료결혈성뇌졸중적분자작용궤제. 방법 장40지SD웅성대서안수궤수자표법분위가수술조、모형조、양성대조조(니막지평조)、은단심뇌통조.니막지평조급은단심뇌통조예선련속관위급약7d,가수술조화모형조매일관복상당량적증류수,제8대제비대서대뇌중동맥조새모형.뇌결혈재관주24 h후응용TUNEL법검측각조대서해마CA1구조망양성신경세포수,응용면역조화염색측정각조대서뇌조직중천동안산특이성반광안산단백매-3(Caspase-3)적표체. 결과 모형조대서균능견도교다적조망양성세포수급Caspase-3양성세포수,여가수술조비교차이유통계학의의(P＜0.05)；여모형조비교,은단심뇌통조、니막지평조능명현감소조망양성세포수급Caspase-3양성세포수,차이유통계학의의(P＜0.05)；은단심뇌통조여니막지평조재조망양성신경세포수급Caspase-3양성세포수상비교차이무통계학의의(P＞0.05). 결론 은단심뇌통대뇌결혈재관주손상유일정보호작용,능구감소뇌결혈재관주대서신경세포적조망,기작용궤제가능여감소뇌조직중Caspase-3적표체유관.
Objective To investigate the protective effects ofYindan Xinnaotong (YDXNT) on neural cell apoptosis in the hippocampus CA1 regions of rats with cerebral ischemia reperfusion and discuss the molecule mechanism of YDXNT treatment in cerebral ischemia.Methods Forty male Sprague-Dawley rats were randomly divided into sham-operated group,model group,positive control group (nimodipine treatment group) and YDXNT treatment group.Prctreatment by continuous intragastric administration for 7 days were given to the rats in the nimodipine treatment group and YDXNT treatment group,while rats in the sham-operated group and model group daily were fed with isovolumic distilled water.Middle cerebral artery models were established by a modified Longa occlusion method in the eighth day.Positive cell population in the hippocampus CA1 region of rats with ischemia 2 h and reperfusion 24 h was marked by TUNEL,and the caspase-3 expression was measured by immunohistochemical method.Results As compared with that in the control group,the number of apoptosis and Caspase-3-positive cells was significantly increased (P＜0.05),decreased number of apoptosis and Caspase-3-positive cells in the YDXNT treatment group and nimodipine treatment group was noted as compared with that in the vihicle group (P＜0.05); however,no difference of them between the nimodipine treatment group and YDXNT treatment group was noted (P＞0.05).Conclusion YDXNT has some protective effect on rats with brain ischemia reperfusion injury,by reducing cell population of apoptosis,whose effect may be related to the reduced expression of Caspase-3.