摘要
目的探讨亚低温对脑缺血/再灌注大鼠细胞骨架蛋白血影蛋白αⅡ(spectrinαⅡ)及卡配因(calpain)、胱冬酶-3(caspase-3)等相关蛋白酶的影响。方法采用线栓法建立大鼠大脑中动脉阻塞(MCAO)及再通模型,将其随机分为假手术组、常温缺血再灌注组(常温组)及亚低温缺血再灌注组(亚低温组),分别于再灌注后不同时间点采用免疫组化法检测各组大鼠血影蛋白αⅡ、卡配因Ⅰ及胱冬酶-3的表达。结果脑缺血再灌注组大鼠梗死灶中心区血影蛋白αⅡ染色消失;梗死灶周围缺血区血影蛋白αⅡ阳性细胞数量呈动态变化过程:再灌注2 h时,脑缺血区血影蛋白αⅡ阳性细胞数量较假手术组开始减少,随着再灌注时间延长,其阳性细胞数量进一步减少,于24 h时达到峰值;与相应常温组相比,亚低温组大鼠血影蛋白αⅡ阳性细胞数量明显大于前者,而卡配因Ⅰ及胱冬酶-3阳性细胞数量则较常温组明显减少。结论亚低温可以抑制局灶性脑缺血再灌注大鼠蛋白酶卡配因Ⅰ、胱冬酶-3的表达,减缓细胞骨架蛋白血影蛋白αⅡ的降解,从而发挥一定程度的脑保护效应。
Objective： To investigate the effects of mild hypothermia （MH） on expression of spectrin αⅡ, calpain Ⅰ and caspase 3 in rats after focal cerebral ischemia reperfusion （ FCIR）, Methods： The rat models of middle cerebral artery occlusion （MCAO） and reperfusion were established by using an intraluminal filament. The rats were randomly divided into a sham-operated group （SO group）, a normothermia ischemia reperfusion group （NIR group） and a mild hypothermia ischemia reperfusion group （ MHIR group）, The expression of Spectrin αII, calpain I and caspase 3 was detected by using immunohistochemistry, Results Spectrin αⅡ positive neurons in peri-infarction region were gradually decreased at 2 h after reperfusion, and reached the peaked at 24 h. Compared with those in the NIR group, the expression of spectrin αⅡ were markedly increased, while the calpain Ⅰ and caspase 3 expression were decreased greatly in the MHIR group, Conclusion The MH neuro-protective effects on FCIR are partly associated with the inhibition of calpain Ⅰ and caspase 3 expression, attenuation of spectrin αII degradation.
出处
《中华物理医学与康复杂志》
CAS
CSCD
北大核心
2007年第4期240-243,共4页
Chinese Journal of Physical Medicine and Rehabilitation
基金
国家自然科学基金(30470585)
黑龙江省自然科学基金(D0309)
黑龙江省教育厅基金(10541117)
