摘要
目的和方法 :利用大鼠在体心肌缺血再灌注模型 ,研究褪黑素对心肌细胞线粒体的保护作用 ,并从氧自由基、钙超载以及能量代谢方面探讨其基本作用机制。结果与结论 :预先给予 10mg/kg的褪黑素能够明显减少再灌注心肌线粒体的丙二醛 (MDA)含量 ,增加还原型谷胱甘肽 (GSH)含量 ,减少钙超载 ,保护线粒体的结构完整性 ,促进再灌注心肌ATP合成能力的恢复 ,维持细胞代谢水平。
AIM and METHODS: To study the protective effect of melatonin on mitochondria of rat myocardium on the ischemia-reperfusion model in vivo, and discuss its mechanism in terms of oxygen free radical, calcium overload and energy metabolism. RESULTS and CONCLUSION: 10 mg/kg melatonin administered 5 min before reperfusion, which obviously reduced the content of malondialdehyde of myocardial mitochondria, increased the content of glutathione, inhibited calcium overload, protected the integrality in mitochondrial structure, promoted the recovery of ability in ATP synthesis after reperfusion, maintained the energy metabolism of the myocardium.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2001年第1期43-45,共3页
Chinese Journal of Pathophysiology
关键词
褪黑激素
线粒体
心肌再灌注损伤
Melatonin
Mitochondria
Myocardial reperfusion injury