摘要
目的 探讨褪黑素对脑缺血后脑细胞线粒体的保护作用及其机制。方法 采用蒙古沙土鼠全脑缺血再灌注模型 ,在沙土鼠双侧颈动脉夹闭前腹腔内注射褪黑素 ,制备药物治疗模型。对照组以生理盐水代替褪黑素。分离前脑线粒体 ,测定线粒体三磷酸腺苷酶 (ATP酶 )活力、线粒体内游离钙水平、线粒体内还原型谷胱甘肽 (GSH)含量等指标。结果 (1)缺血组脑线粒体GSH水平明显降低 ,与药物治疗组和对照组之间存在显著差异 ,而对照组和药物治疗组比较 ,差异无显著性意义 ;(2 )缺血后 1d和 3d组脑线粒体内钙超载 ,与对照组和药物治疗组比较差异显著 ,而对照组和药物治疗组比较 ,差异无显著性意义 ;(3)缺血组脑线粒体Na+,K+ ATP酶和Ca2 +,Mg2 + ATP酶活力与对照组和药物治疗组相比明显降低 ,且随着缺血时间的延长而递降。结论 褪黑素可以提高脑线粒体对缺血、缺氧的耐受性 ,维持脑细胞线粒体结构和功能的稳态 ,保护缺血后的脑细胞。褪黑素对缺血后再灌注的脑神经元有保护作用 ,可能是通过保护线粒体这一环节来实现的。
Objective To investigate the effects of melatonin on mitochondria after cerebral ischemic reperfusion.Methods Carotid artery ligation was used to develop gerbil cerebral ischemic model.For therapeutic group,melatonin was injected 30 minutes before ligation.The activities of ATPase,the free calcium content in mitochondria and the GSH level were measured.Results In the therapeutic group,the activities of ATPase and the GSH level were higher than those in control group,and the free calcium content of mitochondria in the therapeutic group was lower than that in the control group.Conclusions Melatonin can maintain the structure and function of mitochondria,so that it has the neuroprotective effect after cerebral ischemic reperfusion.
出处
《中华老年心脑血管病杂志》
CAS
2000年第5期343-346,共4页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
关键词
脑缺血
线粒体
褪黑素
cerebral ischemia
mitochondria
melatonin
