The administration of complement component C9 augments post-ischemic cerebral infarction volume in neonatal rats.
To determine whether ischemic cerebral infarction is mediated in part by complement component C9, C9-deficient neonatal rats were subjected to unilateral cerebral ischemia. Brains were harvested 24 h later, stained with 2,3,5-triphenyl tetrazolium chloride, and cerebral infarct volumes were quantified by computer-based planimetry. Compared with buffer, prophylactic intraperitoneal (i.p.) administration of the complement inhibitors soluble complement receptor type 1 (sCR1), a molecular hybrid of sCR1 and the selectin inhibitor sialyl Lewis x (sCR1-sLex), or cobra venom factor did not affect the cerebral infarct volume. In contrast, i.p. human C9 (75 microg/g body weight) significantly increased the volume of infarct located 6 through 10 mm posterior to the frontal pole. Therefore, in the post-ischemic brain, C9 was neurotoxic and augmented the focal cerebral infarct volume.
Imm
Mitchell D
MD
Kosair Children's Hospital Research Institute, Department of Pediatrics, Division of Neonatal Medicine, University of Louisville School of Medicine, 571 South Floyd Street, Suite 300, Louisville, KY 40202-3830, USA.
Feldhoff
Pamela W
PW
Feldhoff
Richard C
RC
Lassiter
Herbert A
HA
D000818:Animals; D000831:Animals, Newborn; D002540:Cerebral Cortex / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D002544:Cerebral Infarction / Q000276:immunology* / Q000473:pathology; D003186:Complement C9 / Q000008:administration & dosage / Q000009:adverse effects* / Q000037:antagonists & inhibitors / Q000172:deficiency; D004195:Disease Models, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D011951:Receptors, Complement / Q000378:metabolism; D015427:Reperfusion Injury / Q000276:immunology* / Q000473:pathology
D003186:Complement C9; D011951:Receptors, Complement; C082885:soluble complement inhibitor 1