CAJ | 학술논문

目的观察脑室内亚低温对兔局灶性脑缺血再灌注损伤的保护作用,探讨亚低温对脑缺血性脑损伤脑保护的机制.方法采用线栓法制作兔大脑中动脉闭塞(MCAO)脑缺血模型.将18只新西兰纯种白兔分为对照组、闭塞组、亚低温组.通过脑室内滴注低温液2h后,采用Longa评分法进行神经功能评分评定;按Elliott公式测定脑水肿程度;流式细胞仪检测细胞周期及凋亡率的变化;Western blot法检测半胱氨酰天冬氨酸特异性蛋白酶-3(Caspase-3)蛋白的表达.结果低温组神经功能评分(2.167 ±0.753),明显低于闭塞组(P＜0.01).低温组左侧脑组织干湿比79.26±1.30,与闭塞组、对照组比较于湿比差异有统计学意义(P＜0.05).低温组凋亡率明显降低(2.46±0.84).低温组细胞G1期比例减少(64.05 ±3.24),S期(43.79±2.25)、G2期(12.88±1.77)细胞比例增加,与其他组比较差异有统计学意义(P＜0.01).亚低温下调Caspase-3 17 kb蛋白的表达(P＜0.01).结论亚低温可能通过减轻脑水肿、抑制细胞凋亡、降低脑缺血再灌注后Caspase-3表达,从而发挥其脑保护作用.
목적 관찰뇌실내아저온대토국조성뇌결혈재관주손상적보호작용,탐토아저온대뇌결혈성뇌손상뇌보호적궤제.방법 채용선전법제작토대뇌중동맥폐새(MCAO)뇌결혈모형.장18지신서란순충백토분위대조조、폐새조、아저온조.통과뇌실내적주저온액2h후,채용Longa평분법진행신경공능평분평정;안Elliott공식측정뇌수종정도;류식세포의검측세포주기급조망솔적변화;Western blot법검측반광안선천동안산특이성단백매-3(Caspase-3)단백적표체.결과 저온조신경공능평분(2.167 ±0.753),명현저우폐새조(P＜0.01).저온조좌측뇌조직간습비79.26±1.30,여폐새조、대조조비교우습비차이유통계학의의(P＜0.05).저온조조망솔명현강저(2.46±0.84).저온조세포G1기비례감소(64.05 ±3.24),S기(43.79±2.25)、G2기(12.88±1.77)세포비례증가,여기타조비교차이유통계학의의(P＜0.01).아저온하조Caspase-3 17 kb단백적표체(P＜0.01).결론 아저온가능통과감경뇌수종、억제세포조망、강저뇌결혈재관주후Caspase-3표체,종이발휘기뇌보호작용.
Objective To investigate the protective effect of intraventircle mild hypothermia on focal cerebral ischemia-reperfusion in rabbits and the neuroprotective molecule mechanism.Methods The middle cerebral artery occlusion (MCAO) and reperfusion models of rabbits were achieved by thread embolism.Eighty male rabbits were randomly divided into control group,occlusion group and mild hypothermia group.The neurofunction performance of Longa score and the edema volume of the brain by Elliott method were evaluated,the cells cyle and apoptosis rate were measured by flow cytometry (FCM) and the expression level of cysteinyl aspartate-specific protease-3 (Caspase-3) protein by Western blotting.Results The neurofunctional score in the mild hypothermia group was 2.167 ± 0.753,significantly lower than that in the occlusion group (P ＜ 0.01).Dry-wet weight ratio in mild hypothermia group was 79.26 ± 1.30,which was significantly different from that in occlusion group and control group (P ＜0.01).Flow cytometry revealed that mild hypothermia significantly suppressed apoptosis rate (2.46 ± 0.84).The proportion of cells in G1 phase was declined to (64.05 ± 3.24),and that in S phase and G2 phase was increased to (43.79 ±2.25) and (12.88 ± 1.77) respectively (P ＜0.01).The hypothermia down-regulated Caspase317 kb expression (P ＜0.01).Conclusion The mild hypothermia could reduce brain edema,and inhibit apoptosis by down-regulating the Caspase-3 expression to protect the brain function.