NADPH氧化酶
氧化应激
脑出血
人口
胶原酶
医学
内科学
超氧化物
野生型
内分泌学
化学
酶
生物化学
突变体
基因
蛛网膜下腔出血
环境卫生
作者
Jiping Tang,Jun Liu,Changman Zhou,Dmitry V. Ostanin,Matthew B. Grisham,D. Neil Granger,Junyi Zhang
标识
DOI:10.1111/j.1471-4159.2005.03292.x
摘要
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 gp91phox knockout (gp91phox KO) mice (deficient in gp91phox 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 gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox 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 gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox 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.
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