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

Shao-Peng Lin | Wenjun Li | Ali Winters | Ran Liu | Shao-Hua Yang
Frontiers in cellular neuroscience | 2018

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.

Pubmed ID: 29731711

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Associated grants

  • Agency: NIA NIH HHS, United States
    Id: P01 AG027956
  • Agency: NINDS NIH HHS, United States
    Id: R21 NS087209

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HT22 (tool)

RRID:CVCL_0321

Cell line HT22 is a Transformed cell line with a species of origin Mus musculus (Mouse)

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