Complement activation contributes to XXXX in neonatal @entity35 .

@entity1545 @entity131 @entity2806 @entity63 @entity26 @entity70909 @entity1188 @entity35
Conflicting data have emerged regarding the role of complement activation in the pathophysiology of @entity2806 . On the basis of considerable evidence implicating inflammatory mediators in the progression of neonatal @entity1545 , we evaluated the contribution of complement activation to cerebral @entity63 in the neonatal @entity35 . To elicit unilateral @entity63 , 7-d-old @entity35 underwent right carotid ligation followed by 1.5-2 hr of exposure to 8% @entity26 . Using immunoprecipitation and Western blot assays, we determined that HI induces local complement cascade activation as early as 8 hr post-HI; there was an eightfold increase in the activation fragment inactivated C3b at 16 hr. With immunofluorescence assays and confocal microscopy, both @entity70909 were localized to injured neurons 16 and 24 hr post-HI. To investigate the contribution of systemic complement to @entity1545 , we administered the complement-depleting agent cobra venom factor (CVF) 24 hr before HI lesioning and evaluated both acute HI-induced complement deposition and the extent of resulting tissue injury 5 d after lesioning. CVF depleted both systemic and brain C3 by the time of surgery and reduced @entity1188 size. Analysis of lesioned, CVF-treated animals demonstrated minimal neuronal C3 deposition but no reduction in C9 deposition. C3-immunoreactive microglia were identified in injured areas. These results indicate that complement activation contributes to @entity63 in neonatal @entity35 brain, systemic administration of CVF does not eliminate complement deposition within injured brain, and microglia may represent an important local source of C3 after @entity131 .
