摘要
目的研究脑缺血预处理大鼠脑白细胞介素-6(IL-6)和脑红蛋白(Ngb)的表达及尤瑞克林对其表达的干预作用,探讨脑缺血预处理和尤瑞克林的脑保护机制。方法建立脑缺血及脑缺血预处理大鼠模型,将SD大鼠随机分为脑缺血组、脑缺血预处理组(简称预处理组)和预处理后尤瑞克林干预组(简称干预组)3组,分别于再缺血后12、24、487、2 h观察大鼠神经功能缺损评分、脑梗死体积、海马IL-6和脑皮质Ngb表达变化。结果预处理组脑神经功能缺损评分、梗死体积及海马IL-6阳性表达较脑缺血组降低(P<0.05,P<0.01),干预组较预处理组和脑缺血组均明显降低(P<0.05,P<0.01);预处理组和干预组脑皮质Ngb表达均较缺血组明显增多(P<0.01),但两组间差异无统计学意义。结论脑缺血预处理可对随后发生的再次缺血所致的神经元损伤起保护作用,缺血预处理后使用尤瑞克林可加强脑缺血耐受。
Objective To investigate the neuroprotective mechanism of ischemic preconditioning and kallikrein. Methods 72 healthy male Sprague-Dawley （SD） rats were randomly divided into 3 groups： ischemia group （n= 24）, ischemic preconditioning group （n = 24）, and kallikrein intervention group （n = 24）. Each group was further divided into 4 subgroups according to the time of 12 h, 1 d, 2 d, and 3 d after re-ischemia （each subgroup n=6）. The following indexes in 3 groups were investigated respectively： neurological function, infarct volume and hippocampal IL-6 expression and cortical Ngb expression. Results At the same point of time after ischemia, the score of neurological impairment, the infarct volume and the expression of IL-6 were lower in preconditioning group than those in ischemia group （P〈0.05, P〈0.01）. Moreover, these indexes were much lower in intervention group （P〈0.05, P〈0.01）. The expression of Ngb was higher both in preconditioning group and in intervention group than that in ischemia group （P〈0.01）. However, there was no significant difference between preconditioning group and intervention group. Conclusions Cerebral ischemic preconditioning can protect the brain against the injury of the followed severe isehemia. Application of kallikrein after cerebral ischemia could increase this protection.
出处
《中国神经免疫学和神经病学杂志》
CAS
2009年第1期42-46,共5页
Chinese Journal of Neuroimmunology and Neurology
