Artemisinin, also known as Qinghaosu (Chinese: 青蒿素) is an anti-malarial drug that possess the most rapid action of all the currently available drugs against Plasmodium falciparum malaria. In past three years, we found that artemisinin promoted the survival of various neuronal/non cell types from oxidative insults like H2O2/ SNP and beta amyloid. Pretreatment of PC12 cells with artemisinin significantly suppressed SNP/H2O2/Aβ-induced cell death by decreasing the production of intracellular reactive oxygen species (ROS), preventing the decline of mitochondrial membrane potential, restoring abnormal changes in nuclear morphology and reducing LDH release and caspase 3/7 activities in PC12 cells and D407 cells. Artemisinin was able to stimulate the phosphorylation/activation of different signaling protein such as extracellularly regulated protein kinases (ERK) kinase, AMPK and CREB while it had no effect on the Akt pathway. In addition, inhibitor or siRNA of ERK pathway and AMPK attenuated the protective effects of artemisinin whereas the PI3K inhibitor LY294002 had no effect. Interestingly, intravitreous injection of artimisinin, concentration-dependently reversed the light exposed damage of rat retinal physiological function detected by flash electroretinogram. These results, taken together, suggested that artemisinin is a potential protectant which is able to suppress cell death induced by voxidative stresses. Our results offer support for the potential therapeutic application of artemisinin to prevent neuronal degenerative disorders. Supported by National Natural Science Foundation of China (No. 31771128), MYRG2016-00052-FHS and MYRG2018-00134-FHS from University of Macau, and FDCT 021/2015/A1 and 016/2016/A1).