摘要
目的研究NF-κB与细胞间黏附因子1(ICAM-1)在脑缺血预处理后,诱导脑缺血耐受过程中的作用。方法取100只清洁级Wistar大鼠,随机分为对照组、缺血组、预处理组和缺血预处理组。建立局灶缺血和缺血预处理模型,观察相应时间点大鼠的神经行为学评分、脑梗死体积比、缺血区域NF-κB与ICAM-1的表达情况。结果①缺血组的神经功能缺损评分高于缺血预处理组,脑梗死体积比[(28.6±3.2)%对(16.2±3.8)%,t=2.668]高于缺血预处理组,差异均有统计学意义,P<0.05。②缺血预处理组的NF-κB阳性细胞数量均低于同时间点的缺血组,但高于预处理组,差异有统计学意义,P<0.05;缺血预处理组的阳性细胞数量达高峰时间点延迟为48 h。③缺血预处理组的ICAM-1阳性细胞数量均低于同时间点的缺血组,但高于预处理组,差异有统计学意义,P<0.05。结论缺血预处理可减少缺血后NF-κB、ICAM-1的表达,抑制炎性反应可能是缺血预处理诱导脑缺血耐受的机制之一。
Objective To study the roles of nuclear factor （NF-kB） and intercellular adhesion molecule 1 （ICAM-1） in cerebral ischemic preconditioning induced brain ischemic tolerance. Methods A total of 100 clean rats were randomly allocated into 4 groups： control, ischemic, preconditioning, and ischemic preconditioning groups. Both focal and ischemic preconditioning models were induced. The neuro- ethological score, infarct volume ratio and expression of NF-kB and ICAM-1 in the ischemic region at the corresponding time points were observed. Results （1）The neurological deficit score in the ischemic group was higher than that in the ischemic preconditioning group. The cerebral infarction volume ratio was higher than that in the ischemic preconditioning group （28.6 ±3.2% vs. 16. 2 ±3.8%, t =2. 668[P 〈0. 05] ）, and there were significant differences （ P 〈 0.05 ）. （2）The number of NF-KB positive cells in the ischemic preconditioning group were lower than those in the ischemic group at the same time points, but they were higher than those in the preconditioning group, and there were significant differences（P 〈0. 05）. The peak time of the number of NF-KB positive cells in the ischemic preconditioning group was delayed for 48 hours. （3）The numbers of ICAM-1 positive cells in the ischemic preconditioning group were less than those in the ischemic group at the same time points, but they were higher than those in the preconditioning group, and there were significant differences （P 〈 0. 05 ）. Conclusion Isehemic preconditioning decreases the expression of NF-KB and ICAM-1 after ischemia. The inhibition of inflammatory reaction may be one of the mechanisms of the ischemic tolerance induced by ischemie preconditioning.
出处
《中国脑血管病杂志》
CAS
2010年第7期369-372,共4页
Chinese Journal of Cerebrovascular Diseases
基金
广西自然科学基金资助项目(桂科自0832133)
关键词
缺血预处理
炎性反应
NF—KB
细胞间黏附因子1
大鼠
Ischemic preconditioning
Inflammatory reaction
Nuclear factor
Intercellular adhesion molecule 1
Rats
