Artemisinin prevents glutamate-induced neuronal cell death via Akt pathway activation

Shao Peng Lin, Wenjun Li, Ali Winters, Ran Liu, Shao Hua Yang

Research output: Contribution to journalArticle

9 Scopus citations

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.

Original languageEnglish
Article number108
JournalFrontiers in Cellular Neuroscience
Volume12
DOIs
StatePublished - 20 Apr 2018

Keywords

  • Akt
  • Apoptosis
  • Artemisinin
  • Neuroprotection
  • Oxidative stress

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