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




Lin, Shao-Peng
Li, Wenjun
Winters, Ali
Liu, Ran
Yang, Shaohua


0000-0002-3882-0616 (Liu, Ran)
0000-0002-0405-0887 (Yang, Shaohua)

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Frontiers Media S.A.


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.



Lin, S. P., Li, W., Winters, A., Liu, R., & Yang, S. H. (2018). Artemisinin Prevents Glutamate-Induced Neuronal Cell Death Via Akt Pathway Activation. Frontiers in cellular neuroscience, 12, 108.


© 2018 Lin, Li, Winters, Liu and Yang.


Attribution 4.0 International (CC BY 4.0)