Artemisinin Prevents Glutamate-Induced Neuronal Cell Death Via Akt Pathway Activation

作者：Lin, Shao-Peng^*; Li, Wenjun; Winters, Ali; Liu, Ran; Yang, Shao-Hua^*

来源：Frontiers in Cellular Neuroscience, 2018, 12: 108.

DOI：10.3389/fncel.2018.00108

• artemisinin
• Akt
• oxidative stress
• apoptosis
• neuroprotection

Artemisinin is an anti-malarial drug that has been in use for almost half century. Recently, novel biological effects of artemisinin on cancer, inflammation-related disorders and cardiovascular disease were reported. However, neuroprotective actions of artemisinin against glutamate-induced oxidative stress have not been investigated. In the current study, we determined the effect of artemisinin against oxidative insult in HT-22 mouse hippocampal cell line. We found that pretreatment of artemisinin declined reactive oxygen species (ROS) production, attenuated the collapse of mitochondrial membrane potential induced by glutamate and rescued HT-22 cells from glutamate-induced cell death. Furthermore, our study demonstrated that artemisinin activated Akt/Bcl-2 signaling and that neuroprotective effect of artemisinin was blocked by Akt-specific inhibitor, MK2206. Taken together, our study indicated that artemisinin prevented neuronal HT-22 cell from glutamate-induced oxidative injury by activation of Akt signaling pathway.

• 出版日期2018-4-20
• 单位广州医科大学