The p38-MAPK Pathway Is Involved in Neuroprotection of Artemisinin against H2O2-induced Apoptosis in PC12 Cells

Abstract

Oxidative stress, owing to the excessive production of ROS (reactive oxygen species), is one of the leading causes for the progression of AD (Alzheimer's disease). Increasing evidences suggested that oxidative stress insult impaired the physiological functioning of neuronal cells by inducing cell apoptosis. The search for drug candidates that can effectively protect neurons from oxidative stress insult might hold therapeutic potential for AD. In the present study, we tested the neuroprotective effects and the related action mechanisms of artemisinin, a FDA-approved anti-malarial drug, against H 2 O 2 induced oxidative damage in PC12 cells. It was found that artemisinin reduced cell viability loss caused by hydrogen peroxide (H 2 O 2 ) in PC12 cells. In addition, data from Flow cytometry displayed that artemisinin significantly decreased the apoptosis of PC12 cells induced by H 2 O 2 . Furthermore Western blot analysis displayed that artemisinin stimulated the p38MAPK signaling, while treatment of PC12 cells with specific p38MAPK pathway inhibitor SB203580 blocked the neuroprotective effect of artemisinin. These results together indicated that artemisinin is a potential protectant, and it protects PC12 cells against H 2 O 2 injury through activation of the p38MAPK pathway.