Ｏｂｊｅｃｔｉｖｅ　To investigate the effect of α7 nicotinic acetylcholine receptors agonist(α7nAChR) on brain injury and the expression of NF-κB-p65 induced by CPB, then to clarify its possible mechanism of the protective effects.　Methods　Twenty-four clean male SD rats, weighting of 350-400 g, were randomly divided into four groups (n=6) using a random number table: sham group(group S), CPB group (group C), α7nAChR agonist+CPB group (group P), α7nAChR inhibitor+CPB group (group M). CPB was maintained for 60 min in group C, P and M. Blood and brain sample were collected 2 h after CPB. ELISA was used to detect the changes of serum IL-6, TNF-α, brain injury markers S100β. NF-κB-p65 were detected by Western blot and the morphological changes of hippocampus were observed by hematoxylin and eosin staining.　Results　Compared with group S, the levels of serum S100β, IL-6 and TNF-α in group C, M and P were significantly increased(P<0.05), the expression of NF-κB-p65 were also statistically increased (group S: 0.214±0.031, group C: 0.563±0.093, group P: 0.674±0.097, group M: 0.414±0.074, P<0.05). Compared with group C, the levels of serum above index in group P and M were significantly decrease(P<0.05) and the expression of NF-κB-p65 protein were also statistically decreased(P<0.05). But there was no statistically difference between group M and group C(P>0.05). The morphology of the hippocampus tissues was normal in group S. Clear cellular degeneration and abnormal cell arrangements were observed in group C and M. Compared with group C, the pathological changes of hippocampus were attenuated in group P.　Conclusions　α7nAChR agonists, to some extent, can effectively reduce the brain injury induced by CPB in rats. It may be related to decreased NF-κB-p65 expression, inhibition the inflammatory response triggered by CPB.