Effects of melatonin on mitochondria after cerebral isehemic reperfusion
Melatonin has been regarded as a free radical scavenger and antioxidant. In both in vitro and in vivo experiments. Melatonin was found to protect cells, tissues and organs against oxidative damage induced by a variety of free radical generating agents and processes, e.g., ischemic reperfusion. The mechanisms underlying these interactions have not been defined. The goal of the present study was to observe the effects of melatonin on rnitochondria after cerebral ischemic reperfusion and the mechanisms of neuroprotection of melatonin by gerbil ischemic model. Male Mongolian gerbils were subjected to 10 min of forebrain ischemia by occlusion of both common carotid arteries under anesthesia. Melatonin(0.8 mg/kg) was administrated intraperitoneum 30 min befbre arteries occlusion. We measured the respiratory function of mitochondria, the activities of ATPase, the free mitochondrial calcium contents and the GSH level of mitochondria. The results show that oxidative phosphorylation function of mitochondria was damaged after cerebral ischemic reperfusion. And mitochondrial calcium was overloaded after cerebral ischemic reperfusion. And the level of GSH in mitochondria decreased after cerebral ischemic reperfision. It is concluded that melatonin have neuroprotection effects after cerebral ischemic repertusion and this effects probably related to the protection mitochondria.
oxidative phosphorylation、free radical、respiratory function、radical scavenger、Mongolian gerbils、in vitro
8
S7 ;R72
2005-07-07（万方平台首次上网日期，不代表论文的发表时间）
共1页
79
