摘要
目的探讨二氮嗪预处理对幼龄大鼠深低温脑缺血/再灌注损伤脑保护作用。方法将3周龄SD大鼠90只随机分为假手术组、模型组及二氮嗪组,缺血/再灌注后1、6、24、72h和7d,建立深低温脑缺血/再灌注模型,采用免疫组织化学检测不同时点脑组织细胞色素C的蛋白表达,并观察脑组织病理变化。结果与假手术组比较,模型组于再灌注后6和24h显示明显的病理变化,其脑组织胞浆细胞色素C于灌注后6h后即明显升高(P<0.05),24h达到高峰(P<0.01)。二氮嗪组病理改变较轻,细胞色素C含量于再灌注后24和72h显著低于模型组(P<0.05)。结论二氮嗪预处理可抑制线粒体细胞色素C的释放,对幼龄大鼠深低温脑缺血/再灌注损伤具有一定脑保护作用。
Objective To determine the effects of diazoxide on a model of brain injury induced by deep hypothermic cerebral ischemia/reperfusion （I/R）. Methods Ninety-three week-old Sprague- Dawley rats were randomly and equally divided into sham operation group, model group and diazoxide group. Each group was redistributed into five subgroups of 1, 6, 24, 72 hours and 7 days after reperfusion. The expression of cytochrome C was determined by immunohistochemistry. The pathological change of the brain was observed by HE staining. Results The model group had the characteristic changes of I/R injury. The expression of cytochrome C was increased from 6 to 72 hours after reperfusion more in model group than that in sham operation group （P〈0. 05 or P〈0. 01）. The diazoxide group had less pathological injury than the model group, and markedly inhibition of cytochrome C release at 24 and 72 h after reperfusion （P〈0.05 or P〈0.01）. Conclusion The results suggest that diazoxide has a protective effect against deep hypothermic cerebral I/R injury through inhibiting mitochondrial cytochrome C release.
出处
《江苏医药》
CAS
CSCD
北大核心
2008年第3期248-250,I0003,共4页
Jiangsu Medical Journal
基金
国家自然科学基金(30772156)
江苏省医学重点人才基金
江苏省社会发展项目资金(BS2002306)
关键词
二氮嗪
深低温
脑缺血/再灌注损伤
细胞色素C
Diazoxide
Deep hypothermia
Cerebral ischemia/reperfusion injury
Cytochrome C
