Objective To observe the effect of electroacupuncture (EA) of "Baihui" (GV 20) and left "Hegu" (LI 4)-"Taichong" (LR 3) on levels of hippocampal IL-1β content and I kappa B kinase (IKK) β protein in focal cerebral ischemia/reperfusion (Cl/R) injury rats so as to reveal its mechanism underlying improvement of cerebral ischemia.Methods One hundred and ninety-eight male SD rats were randomly divided into sham group (n=54),model group (n=72) and EA group (n=72) which were further randomized into 12 h,24 h and 48 h subgroups according to the duration of CI/R.The focal CI/R injury model was established by middle cerebral artery occlusion (MCAO) and reperfusion.EA (1 mA,2 Hz/100 Hz) was applied to "Baihui" (GV 20) and the left "Hegu" (LI 4)-"Taichong" (LR 3) for 20 min,once every 12 h.The level of IL-1β content in the right hippocampus tissue was detected by ELISA and the expression levels of hippocampal IKKβ protein were detected by immunohistochemistry and Western blot,respectively.Results Compared with the 3 subgroups of the sham group,the levels of hippocampal IL-1β contents at time-points of 12 h,24 h and 48 h after MCAO were significantly increased in the model group (P＜0.01).In comparison with the model group,the contents of hippocampal IL-1β at the 3 corresponding time-points in the EA group were significantly reduced (P＜0.01).The expression levels of hippocampal IKKβ protein at the 3 time-points after MCAO shown by immunohistochemistry and Western blot analysis were significantly higher in the model group than in the sham group (P＜0.05),and considerably lower in the EA group than in the model group (P＜0.05).Conclusion EA of GV 20 and LI 4-LR 3 can obviously reduce Cl/R injury induced increase of IL-1β content and IKKβ expression level in the hippocampus,which may be responsible for its effect in alleviating cerebral infarction by reducing inflammatory injury in the hippocampus.%目的:观察局灶性脑缺血再灌注后大鼠右侧海马内白介素1β(IL-1β)及转录核因子κcB抑制蛋白激酶β(IKKβ)的变化及电针对其的调节作用,探讨局灶性脑缺血再灌注后大鼠海马内炎性反应的活化及电针对大鼠海马内炎性反应损害的抑制作用的可能机制.方法:将SD雄性大鼠随机分为假手术组(n=54)、模型组(n=72)、电针组(n=72),按照再灌注后12h、24h及48 h分成3个亚组.改良线栓法制备右侧大脑中动脉闭塞再灌注模型.电针组选“百会”穴及左侧“四关”穴(2 Hz/100 Hz,1 mA),每次电针20 min,3个亚组分别电针2、3、4次.运用ELISA法检测IL-1β在海马中的含量,免疫组化及Western blot法检测IKKβ在缺血侧海马内的蛋白表达.结果:模型组大鼠海马中IL-1β含量较假手术组明显增加(P＜0.01)；与模型组比较,电针组IL-1β含量显著下降(P＜0.01).模型组IKKβ蛋白表达较假手术组显著升高(P＜0.05),电针干预后能明显抑制IKKβ在海马内的蛋白表达(P＜0.05).结论:局灶性脑缺血再灌注损伤后大鼠海马内出现炎性变化,电针干预能减少IL-1β含量,降低IKKβ在海马区的蛋白表达,有利于缓解脑缺血海马内的炎性反应损害.
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