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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 investigate the role of NF-κB and intercellular adhesion molecule-1 (ICAM-1) in inducing cerebral ischemic tolerance after cerebral ischemic preconditioning. Methods 100 clean Wistar rats were randomly divided into control group, ischemia group, preconditioning group and ischemic preconditioning group. The model of focal ischemic and ischemic preconditioning was established. The neurobehavioral score, the volume ratio of cerebral infarction, the expression of NF-κB and ICAM-1 in ischemic area were observed at the corresponding time points. Results ① The score of neurological deficit in ischemic group was higher than that of ischemic preconditioning group, the volume ratio of cerebral infarction was (28.6 ± 3.2)% vs (16.2 ± 3.8)%, t = 2.668] All were statistically significant, P <0.05. ② The number of NF-κB positive cells in ischemic preconditioning group was lower than that of ischemia group at the same time point, but higher than that of pretreatment group, the difference was statistically significant, P <0.05; the number of positive cells in ischemic preconditioning group The peak time delay is 48 h. ③ The number of ICAM-1 positive cells in ischemic preconditioning group was lower than that in ischemia group at the same time point, but higher than that in preconditioning group, the difference was statistically significant (P <0.05). Conclusion Ischemic preconditioning can reduce the expression of NF-κB and ICAM-1 after ischemia, and inhibiting the inflammatory reaction may be one of the mechanisms of ischemic preconditioning-induced cerebral ischemic tolerance.