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Role of NADPH oxidase in the brain injury of intracerebral hemorrhage
Author(s) -
Tang Jiping,
Liu Jun,
Zhou Changman,
Ostanin Dmitry,
Grisham Matthew B.,
Neil Granger D.,
Zhang John H.
Publication year - 2005
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2005.03292.x
Subject(s) - nadph oxidase , oxidative stress , intracerebral hemorrhage , population , collagenase , medicine , superoxide , wild type , endocrinology , chemistry , enzyme , biochemistry , mutant , gene , environmental health , subarachnoid hemorrhage
The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension‐ and aging‐induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild‐type C57BL/6 and gp91 phox knockout ( gp91 phox KO) mice (deficient in gp91 phox subunit of the superoxide‐producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91 phox KO mice than wild‐type mice. Total oxidative product was lower in gp91 phox KO mice than in wild‐type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild‐type but not in gp91 phox KO mice. This ICH‐induced brain injury in wild‐type mice is associated with enhanced expression of the gp91 phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury.