[Influence of electroacupuncture intervention on hippocampal IL-1beta content and I kappa B kinase beta expression in focal cerebral ischemia/reperfusion rats].Zhen Ci Yan Jiu 2013; 38(4):271-6ZC
To observe the effect of electroacupuncture (EA) of "Baihui" (GV 20) and left "Hegu" (LI 4)-"Taichong" (LR 3) on levels of hippocampal IL-1beta content and I kappa B kinase (IKK) beta protein in focal cerebral ischemia/reperfusion (CI/R) injury rats so as to reveal its mechanism underlying improvement of cerebral ischemia.
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-1beta content in the right hippocampus tissue was detected by ELISA and the expression levels of hippocampal IKKbeta protein were detected by immunohistochemistry and Western blot, respectively.
Compared with the 3 subgroups of the sham group, the levels of hippocampal IL-1beta 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-beta at the 3 corresponding time-points in the EA group were significantly reduced (P < 0.01). The expression levels of hippocampal IKKbeta 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).
EA of GV 20 and LI 4-LR 3 can obviously reduce CI/R injury induced increase of IL-1beta content and IKKbeta expression level in the hippocampus, which may be responsible for its effect in alleviating cerebral infarction by reducing inflammatory injury in the hippocampus.