摘要
目的探讨肢体缺血预处理(limb ischemic preconditioning,LIP)对大鼠缺血再灌注海马HSP70表达的影响。方法将66只凝闭椎动脉大鼠随机分为假手术组、脑缺血组和LIP+脑缺血组,后两组根据脑缺血后再灌流时间不同进一步分为1、62、4、72和120 h组。采用免疫组织化学方法检测海马HSP 70的变化。结果假手术组海马各区未见明显的HSP70表达。脑缺血组海马CA1区未见明显着色,但在CA3区及齿状回颗粒细胞中可见HSP70着色,以再灌注后24 h最明显。在LIP+脑缺血组,海马CA1区于再灌注1 h未见明显的HSP70表达;再灌注6 h HSP70表达明显增强,与假手术组和脑缺血6 h组比较,阳性细胞数明显增加(P<0.01);再灌注24 h HSP70表达达高峰;再灌注72 h HSP70表达有所下降;至再灌注120 h HSP70表达明显下降。结论损伤性脑缺血前给予LIP,可明显增加CA1区HSP70的阳性表达,诱导CA1区锥体细胞耐受缺血损伤。
Objectlve To determine the effect of limb ischemic preconditioning（LIP） on HSP70 expression in the hippocampus after cerebral ischemia-reperfusion. Methods Sixty-six Wistar rats with vertebral arteries permanently occluded were divided into sham operation group, cerebral ischemic group and LIP ＋ cerebral ischemic group. The two latter groups were further divided into 1, 6, 24, 72 and 120 h groups according to the time of reperfusion after cerebral ischemia respectively. Changes in the expression of HSP70 in the hippocampus were observed using immunohistoehemistry method. Results It was found that there was no obvious HSP 70 positive expression in every subfield of hippoeampus in sham operation group. In cerebral isehemic group, HSP70 expression was found in the CA3 subfield and dentate gyms but not in the CA1 subfield. In LIP ＋ cerebral isehemic group,no HSP70 expression was found in the hippocampus CA1 1 h after cerebral ischemia. but the HSP70 expression was increased at 6 h, and obviously enhanced 24 h after cerebral ischemia, in which the number of positive cells was significantly higher than that in sham operation group and cerebral ischemia 24 h group（ P 〈 0.01）. The expression became very weak 120 h after cerebral ischemia. Conclusion LIP could induce the increase in HSP70 expression in the hippocampus CA1, suggesting that HSP70 might play a role in the induction of brain ischemic tolerance induced by LIP.
出处
《中华老年心脑血管病杂志》
CAS
北大核心
2006年第6期416-419,共4页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
关键词
脑缺血
缺血预处理
再灌注损伤
热休克蛋白质70
海马
大鼠
brain ischemia
ischemia preconditioning
reperfusion injury
heat-shock proteins 70
hippocampus
rats
