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

  • Front Cell Neurosci. 2018 Apr 20;12:108. doi: 10.3389/fncel.2018.00108.
Shao-Peng Lin  1  2 Wenjun Li  1 Ali Winters  1 Ran Liu  1 Shao-Hua Yang  1
Affiliations
  • 1. Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX, United States.
  • 2. Department of Emergency, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
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.

Keywords
Akt; apoptosis; artemisinin; neuroprotection; oxidative stress.
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