Reduced tissue damage and improved recovery of motor function after traumatic brain injury in mice deficient in complement component C4.

摘要: Complement component C4 mediates C3-dependent tissue damage after systemic ischemia—reperfusion injury. Activation of C3 also contributes to the pathogenesis experimental and human traumatic brain injury (TBI); however, few data exist regarding specific pathways (classic, alternative, lectin) involved. Using complement knockout mice a controlled cortical impact (CCI) model, we tested hypothesis that classic pathway secondary TBI. After CCI, C4c C3d immunostaining were detected in vascular endothelial cells wild-type (WT) mice; C1q−1/− mice, was C4−/− mice. WT had similar motor deficits, Morris water maze performance, lesion size. Naive did not differ baseline but reduced postinjury deficits (days 1 7, P < 0.05) decreased 14 ...