artemisinin prevents glutamate-induced neuronal cell death via akt pathway activation

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ID: 225942
2018
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Abstract
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.
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lin2018frontiersartemisinin Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Shao-Peng Lin, Wenjun Li, Ali Winters, Ran Liu, Shao-Hua Yang
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Journal macromolecular bioscience
Year 2018
DOI
10.3389/fncel.2018.00108
URL
http://journal.frontiersin.org/article/10.3389/fncel.2018.00108/full
Keywords
apoptosis oxidative stress artemisinin akt neuropsychiatry biological psychiatry

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