To observe the expression levels of the complement fragment C1q and C3c in rat brain tissues with cerebral ischemia-reperfusion (I/R) injury, and explore the correlation, roles and mechanism of complement reaction and microglia in the brain I/R injury.A total of 48 male Sprague-Dawley rats were randomly divided into normal control group, sham group, I/R 24 h, 72 h, 7 d, 15 d model groups. Suture occlusion method was operated to establish focal middle cerebral artery occlusion (MCAO) and reperfusion models. The Nissl staining was applied to observe the structure of neurons, and immunohistochemistry was applied to detect CD11b, C1q and C3c expression.Compared with the sham group, Nissl staining reaction in brain tissues was stronger in the I/R 24 h group, and then became weaker, and the reduction was the most significant in the I/R 72 h group. The expression of CD11b protein increased in the I/R 24 h group and reached the peak value in the I/R 72 h group, followed by gradually reducing. Compared with the sham group, all the model groups were significantly stronger in CD11b expression (P<0.05). C1q and C3c sharply increased in the brain tissue of I/R 24 h group and peaked in the I/R 7 d group, and then presented a downward trend; the differences between the sham group and all the model groups were of statistical significance (P<0.05).The expression levels of C1q and C3c are positively correlated with CD11b protein in rat brain tissues with cerebral I/R injury, suggesting that cerebral I/R injury inintiate the brain innate immune response, activates complement C1q and C3c as well as microglia, thus playing the role of protection or damage in cerebral I/R injury.