摘要
目的:研究氢生理盐水(HS)对大鼠缺血再灌注肝细胞线粒体功能的保护作用并探讨其可能机制。方法:将雄性SD大鼠随机分为3组(n=14),除假手术组外,均采用阻断左中肝蒂造成缺血再灌注模型,不同组大鼠分别给予等量生理盐水和HS(5 ml/Kg,i.p.),再灌注180min后分别检测其线粒体功能及线粒体MDA、GSH/GSSH变化情况,电镜观察各组大鼠肝细胞线粒体的形态学改变。结果:缺血再灌注后,大鼠线粒体功能出现明显损伤,HS组肝细胞线粒体功能及线粒体氧化损伤程度明显轻于对照组(P<0.01)。电镜观察缺血再灌注后,肝细胞线粒体出现明显损伤,HS组病理改变明显轻于对照组。结论:HS能显著减轻缺血再灌注大鼠肝细胞线粒体损伤,并能有效抑制线粒体氧化应激。
Objective：To study the effect of hydrogen-rich saline on the prevention of liver mitochondrial injury induced by isch -emia-reperfusion （I/R） in rats. Methods：Male Sprague-Dawley rats （n=42） were randomly divided into three experimental groups （ n=14）, namely, sham-operated, I/R plus saline-treated （5 mL/kg, i.p.）, and I/R plus hydrogen-rich saline-treated （5 mL/kg, i.p.） groups. Mi-tochondrial oxidative stress and functions, as well as morphologic changes in the mitochondria, were detected 180 min after reperfu -sion. Results：After I/R, mitochondrial swelling and vague cristae were observed. Mitochondrial functions were significantly decreased, but mitochondrial MDA and GSSH contents were increased by I/R. Hydrogen-rich saline reduced these markers, improved mitochondri-al ATP content and respiratory function, and relieved morphological mitochondrial injury （P〈0.01）. Conclusion：Hydrogen-rich saline attenuated I/R-induced liver mitochondrial damage and reduced mitochondrial oxidative stress.
出处
《中国肿瘤临床》
CAS
CSCD
北大核心
2014年第2期98-101,共4页
Chinese Journal of Clinical Oncology
关键词
氢生理盐水
缺血再灌注
线粒体功能
氧化应激
hydrogen-rich saline, ischemia-reperfusion, mitochondrial function, oxidative stress
