Artemisinin is an anti-malarial drug that possess the most rapid action of all the currently available drugs against Plasmodium falciparum malaria. It is clinically safe, potent and effective in humans. At present, we found that artemisinin promoted the survival of various cell types such as PC12 cells and primary cortical cultured neurons from oxidative insults. For example, pretreatment of PC12 cells with artemisinin significantly suppressed SNP/H2O2-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 and caspase 3/7 activities. Western blot analysis showed that artemisinin was able to stimulate the phosphorylation/activation of extracellular regulated protein kinases (ERK) kinase and CREB while had no effect on the Akt pathway. In addition, the ERK signaling pathway inhibitors or knockdown the expression of ERK protein attenuated the protective effect of artemisinin whereas the PI3K inhibitor LY294002 had no effect. Taken together, these results suggested that artemisinin is a potential protectant which is able to suppress various oxidative stresse’s induced cell death via the activation of ERK signaling. In addition, our current data showed that artemether improved the recognition deficit of AD mice. These results offer support for the potential therapeutic application of artemether to prevent neuronal degenerative disorders like Alzheimers Disease.