引用本文:吕 鹏,李 玲,张 丽.大鼠全脑缺血对再灌注海马区NO含量和Bcl-2表达的影响[J].大连医科大学学报,2009,31(6):649-652.
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大鼠全脑缺血对再灌注海马区NO含量和Bcl-2表达的影响
吕 鹏1, 李 玲1, 张 丽2
1.大连医科大学 附属第二医院 实验中心,辽宁 大连116027;2.大连医科大学 病原学实验室,辽宁 大连116044
摘要:
[目的]探讨全脑缺血预处理对再灌注海马区NO含量和Bcl-2表达的影响。[方法]将72只Wistar大鼠随机分为假手术组、脑缺血组和脑缺血预处理组。假手术组:仅暴露4条血管。脑缺血组:四动脉阻断法,全脑缺血10 min。脑缺血预处理组:全脑缺血预处理3 min,再灌注24 h后再次全脑缺血10 min。所有动物均于末次脑缺血再灌注后12、24、48和72 h取脑组织海马区,硝酸还原酶法检测NO2./NO3.含量,间接反应NO含量;免疫组化方法测定海马区Bcl-2表达。[结果]与假手术比较,脑缺血组和脑缺血预处理组NO含量明显增加,脑缺血组NO含量在48 h达到高峰,72 h出现回落;脑缺血预处理组NO含量在各时间点的变化趋势不明显,与脑缺血组在48和72 h比较差异性有显著性意义(P<0.05,P<0.01)。脑缺血组和脑缺血预处理组Bcl-2表达与假手术组比较明显升高;脑缺血组Bcl-2表达24 h达到高峰,48 h开始减少;脑缺血预处理组Bcl-2表达在12 h表达开始增加,48 h达到高峰,72 h开始减少;在48和72 h,脑缺血预处理组Bcl-2表达明显高于脑缺血组(P<0.05,P<0.01)。[结论]脑缺血预处理引起的NO含量增加,可能与Bcl-2上调表达增加及高峰延迟具有一定相关性。
关键词:  全脑缺血  脑缺血预处理  一氧化氮  Bcl-2  海马区
DOI:10.11724/jdmu.2009.06.06
分类号:R743
基金项目:
Effects of global cerebral ischemic precondition on NO content and Bcl-2 expression in reperfusion of hippocampus
Lü Peng1, LI Ling1, ZHANG Li2
1.Central Laboratory, the Second Affiliated Hospital of Dalian Medical University, Dalian 116027, China;2.Dalian Medical University, Dalian 116044, China
Abstract:
[Objective] To observe the effects of global cerebral ischemic precondition on NO content and Bcl-2 expression in the reperfusion of the hippocampus. [Methods] Seventy-two rats were randomly divided into three groups. The rats sham-operated were only explored four vessels,and global ischemia was induced by occluding four vessels for 10 minutes. In ischemic precondition group, the rats firstly subjected 3-min global ischemia and then after 24 hours, repeated ischemia sustained for 10 minutes. At 12, 24, 48 and 72 h after reperfusion, the hippocampus was removed. The NO content and Bcl-2 expression of hippocampus were respectively measured by the method of nitrate reductase and immunohistochemistry. [Results] Comparing with sham-operated group, NO content enhanced in global ischemic or ischemia precondition group. In ischemic group, the NO content remarkably increased in 48 h and decreased in 72 h, and was significant higher at 48 h and 72 h comparing with ischemic precondition group (P<0.05, P<0.01). The expressions of Bcl-2 in global ischemic and ischemia precondition groups were higher than sham-operated group. In ischemic group, Bcl-2 expression was remarkably increasing at 24 h and decreasing at 48 h (P<0.05, P<0.01), but in ischemic precondition group, it increased at 48 h and decreased at 72 h. Bcl-2 expression was significant lower in ischemic group than that in ischemic precondition group at 48 h and 72 h (P<0.05; P<0.01). [Conclusion] In some extent,the increase of NO content may be related with up-regulated expression of Bcl-2 and delayed peak level in ischemic precondition.
Key words:  global cerebral ischemia  cerebral ischemic precondition  nitric oxide  Bcl-2  hippocampus