摘要
目的:探讨环孢素对癫痫大鼠海马氧化应激、线粒体膜通透性及能量代谢的影响及机制。方法:应用匹鲁卡品建立癫痫持续状态模型,检测癫痫大鼠海马在环孢素干预前后丙二醛和超氧化物歧化酶的变化;检测癫痫大鼠海马在环孢素干预前后线粒体膜通透性转换、线粒体呼吸链复合物I和III活性及ATP含量的变化。结果:环孢素抑制癫痫大鼠海马组织线粒体膜通透性转换;明显降低癫痫大鼠海马组织丙二醛的含量,提高超氧化物歧化酶的活性(P<0.05);明显增加癫痫大鼠海马组织线粒体呼吸链复合物I活性(P<0.05),而对粒体呼吸链复合物III活性无显著影响;明显增加癫痫大鼠海马组织ATP的含量(P<0.05)。结论:环孢素能抑制癫痫大鼠海马氧化应激反应,减轻癫痫大鼠线粒体能量代谢损伤。
AIM： To investigate the effects of cyclosporin on oxidative stress and mitochondrial energy metabo- lism in the rat hippocampus after status epilepticus. METHODS： Status epilepticus was induced by pilocarpine. The changes of malondialdehyde and superoxide dismutase in the rat hippocampus with or without cyclosporin injection were evaluated. Additionally, the mitochondrial permeability transition, the activity of mitochondrial respiratory chain complex I/III and ATP content in the rat hippocampus were detected. RESULTS： Cyclosporin significantly inhibited mitochondrial permeability transition in the rat hippocampus after status epilepticus. Decreased mallondialdehyde and increased superoxide dismutase levels were detected in cyclosperin treatment group compared with status epilepticus group （ P 〈 0.05 ）. More- over, the activity of mitochondria respiratory chain complex I, not III, in the mitochondrial fraction increased after cyclo- sporin treatment （P 〈 0.05）. In addition, cyclosporin significantly prevented the decrease of ATP content in rat hippocam- pus after status epilepticus （P 〈 0.05）. CONCLUSION： Cyclosperin suppresses oxidative stress in the rat hippocampus after status epilepticus. Cyclosporin alleviates the impairment of mitochondrial energy metabolism in rat hippocampus after status eoileoticus.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2014年第1期117-120,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.81000557)
山东大学自主创新基金资助项目(No.2012TS145)
关键词
癫痫
环孢素
氧化性应激
线粒体
能量代谢
Epilepsy
Cyclosporin
Oxidative stress
Mitochondria
Energy metabolism
