褪黑素通過增強自噬保護(hù)缺血再灌注損傷的N2a.pdf

1、Researches have shown that melatonin is neuroprotectant in ischemia/reperfusion-mediated injury. Although melatonin is known as an effective antioxidant，themechanism of the neuroprotection cannot be explained merely by i

2、ts antioxidation.Our study was devoted to explore other existing mechanisms by investigating whethermelatonin protects ischemia/reperfusion-injured neurons through elevating autophagy,since autophagy has been frequently

3、suggested to play a crucial role in neuronsurvival. To find it out，an ischemia/reperfusion model in N2a cells was establishedfor examination by MTT，TEM，LCSM and Western Blotting. The results showed thatautophagy was sign

4、ificantly enhanced in N2a cells treated with melatonin atreperfusion onset following ischemia and cell viability was remarkably increased,while autophagy blockage by 3-MA led to decreased N2a cell survival. Besides,class

5、ic antioxidant Vitamin C was not as strong as melatonin in promoting cellsurvival. It was also observed that rapamycin，an autophagy activator，greatlyactivated autophagy but did not promote cell survival as did melatonin.