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BACKGROUND: Nuclear factor-KB (NF-KB), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in brain tissue can participate in inflammatory reactions after cerebral ischemia. Acupuncture treatment for acute cerebral ischemia produces abnormal protein expression.OBJECTIVE: To investigate the effects of acupuncture on NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the brain tissue of rats with cerebral ischemia/reperfusion injury. DESIGN, TIME AND SETrlNG: Randomized, controlled, animal experiments were performed at the Laboratory of Department of Neurosurgery, Xiangya Hospital, Central South University, China between December 2008 and October 2009.MATERIALS: Rabbit anti-NF-KB polyclonal antibody, rabbit anti-ICAM-1 polyclonal antibody, and rabbit anti-VCAM-1 polyclonal antibody were purchased from Santa Cruz Biotechnology, USA. METHODS: A total of 46 healthy, Sprague Dawley rats were randomly assigned to sham surgery (n = 10), model (n = 12), acupuncture pretreatment (n = 12), and acupuncture intervention (n = 12) groups. Models of middle cerebral artery occlusion were established by right common carotid artery ligation. In the acupuncture pretreatment group, rats received acupuncture for 3 consecutive days, and then models were established. In the acupuncture intervention group, rats acupuncture for 3 consecutive days at Waiguan (SJ 5), Sanyinjiao (SP 6), and Dazhui (DU 14) acupoints following model establishment.MAIN OUTCOME MEASURES: Somatosensory asymmetry and forelimb use asymmetry were tested, as well as NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex at 4, 12, 24, 48 and 72 hours following cerebral ischemia/reperfusion injury. RESULTS: Acupuncture improved neurological function and significantly decreased NF-kB, ICAM-1, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex of rats with cerebral ischemia/reperfusion injury (P < 0.05). CONCLUSION: Acupuncture can improve neurological function, potentially via inhibition of NF-KB, ICAM=I, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex of rats with cerebral ischemia/reperfusion injury.