摘要
目的研究全脑缺血再灌注损伤后ERK在SD大鼠海马的表达及热休克预处理对其表达的影响,以阐明ERK在脑缺血再灌注损伤中作用机制.方法健康雄性SD大鼠90只,随机分为假手术组(SO组,n=30),缺血再灌注组(IR组,n=30),热休克预处理组(HSP组,n=30),以四血管法建立全脑缺血再灌注模型,将大鼠置于42℃中15min行热休克预处理,全脑缺血6min后2,6,12,24h,3,5d再灌注后处死,取海马组织行HE染色,ERK免疫组化染色,TUNEL法检测凋亡细胞.结果IR缺血再灌注后2hERK在CA1区开始表达,24h达到高峰,5d仍有表达,CA3区弱于CA1区,同时CA1区细胞损伤明显,HSP组ERK在CA1和CA3区相应时点均弱于IR组(P<0.05),细胞损伤轻微,凋亡细胞减少(P<0.05).结论全脑缺血再灌注损伤后ERK过度表达参与了神经元损伤过程,热休克预处理通过下调ERK过度表达具有脑保护作用.
AIM ： To investigate the expression of ERK in hippocampus of SD rats after global cerebral ischemia/reperfusion and the effect of heat shock preconditioning on it, and to clarify the role of ERK in global cerebral ischemia/reperfusion injury. METHODS： Ninety healthy male SD rats were divided into 3 groups randomly ： sham operation group （ SO group, n = 30）, ischemia/reperfusion group （IR group, n = 30 ） and heat shock preconditioning group （ HSP group, n = 30）. Global cerebral ischemia/reperfusion model was produced by 4-VO method. The rats were put in 42℃ for 15 min as heat shock preconditioning, then subjected to 6 min ischemia followed by 2, 6, 12, 24 h, 3, 5 d reperfusion, and all rats were executed at corresponding time points. HE staining, immunohistochemical staining and TUNEL staining of brain tissue section were performed. RESULTS： In CAI of IR group, ERK was expressed 2 h after global cerebral ischemia/reporfusion, peaked at 24 h and still lasted at 5 d. Expression in CA3 was weaker than that in CAI and cellular damage in CAI was more obvious. Expression of ERK in CAI and CA3 of HSP group were weaker than that in IR group at each time points （P 〈 0.05 ）. At the same time, cellular damage was weaker and apoptotic cells decreased （ P 〈 0.05 ）. CONCLUSION ： Overexpression of ERK after global cerebral ischemia/reperfusion participated in the neuronal injury procedure and heat shock preconditioning exerted its brain protective function through its suppressive effect on the overexpression of ERK.
出处
《第四军医大学学报》
CAS
北大核心
2006年第16期1449-1452,共4页
Journal of the Fourth Military Medical University
基金
陕西省科技攻关项目[2005K13-G4(1)]
关键词
脑缺血
再灌注损伤
热休克预处理
细胞外信号调节MAP激酶类
brain ischemia
reperfusion injury
heat shock pre conditioning
extracellular signal-regulated MAPkinases
