[Effect of scalp acupuncture on the expression of NF-kappaB mRNA, COX-2 mRNA and their proteins in rats with acute cerebral ischemia-reperfusion injury].

Objective: To explore the possible mechanism of scalp acupuncture (SA) in relieving cerebral ischemia reperfusion (CI-R) injury.
Methods: Seventy male SD rats were randomized into sham-operation (sham, n = 10), model (n = 30) and SA (n = 30) groups. The later 2 groups were further divided into 24 h, 48 h and 72 h subgroups respectively, with 10 cases in each. CI-R model was established by middle cerebral artery occlusion (MCAO) and reperfusion. Electroacupuncture (2 mA, 2 Hz/100 Hz) was applied to "Dingnie Houxiexian" (MS 7) and "Dingnie Qianxiexian" (MS 6) for 30 min, once every 24 h. Changes of the animal behavior were observed by using neurological severity score (NSS), nuclear factor-kappa B (NF-kappaB) and cyclooxygenase (COX-2) contents and their mRNA expression were detected with enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR) techniques respectively.
Results: Following modeling, the NSS at 24 h, 48 h and 72 h after MCAO increased significantly, while compared with model group, NSS of SA group at the 3 time-points decreased considerably (P < 0.05, P < 0.01), suggesting an improvement of the neurological functions after SA treatment. In comparison with sham group, NF-kappaB mRNA and COX-2 mRNA, and NF-kappaB and COX-2 protein expression of model group in the infarcted cerebral tissue were significantly upregulated at the 3 time-points (P < 0.01) except NF-KB mRNA at 72 h (no significant change), while compared with the 3 time-points of model group, NF-kappaB mRNA and COX-2 mRNA, and NF-KB and COX-2 protein expression of SA group were downregulated obviously (P < 0.01) except COX-2 mRNA at 72 h.
Conclusion: Scalp acupuncture can suppress cerebral ischemia-induced upregulation of NF-kappaB mRNA and COX-2 mRNA, and NF-kappaB and COX-2 protein expression, which may contribute to its effect in promoting neurofunctional rehabilitation of CI-R rats by reducing cytokines-mediated inflammatory reaction.