Artemisinin Protects Oxidative Stress-induced Neuronal Apoptosis Via Up-Regulation of Akt/Bcl-2 Signaling

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dc.contributor.authorLiu, Ran
dc.contributor.authorXie, Luokun
dc.contributor.authorLi, Wenjun
dc.contributor.authorWinters, Ali
dc.contributor.authorChaudhari, Kiran
dc.contributor.authorPrah, Jude
dc.contributor.authorYang, Shao-Hua
dc.creatorLin, Shao-Peng
dc.date.accessioned2019-08-22T20:03:58Z
dc.date.available2019-08-22T20:03:58Z
dc.date.issued2017-03-14
dc.date.submitted2017-02-20T08:52:44-08:00
dc.description.abstractPurpose: Artemisinin is a powerful anti-malarial drug that has been in use for decades. Recently, the novel biological effects of artemisinin on cancer, inflammation-related disorders, and cardiovascular disease were reported. The aim of this study was to explore the neuroprotective actions of artemisinin. Methods: The model of glutamate-induced oxidative injury in HT22 hippocampal cells was established to simulate cellular ischemic model. We investigated the effect of artemisinin on oxidative stress-induced cell apoptosis death and the activity of Akt/Bcl-2 pathway in HT22 cells. Results: Pretreatment with artemisinin attenuated reactive oxygen species (ROS) generations, preventing the decline of mitochondrial membrane potential and rescued the HT22 cells form glutamate-induced apoptosis death. The Akt/Bcl-2 pathway was activated by artemisinin in time dependent manner. Furthermore, the artemisinin inhibitor MK2206 blocked the neuroprotective effect of artemisinin. Conclusions: Artemisinin protects neuronal HT22 cell from glutamate-induced oxidative injury and apoptosis via Akt/Bcl-signaling, thereby might be applicated for clinical neurological therapy.
dc.identifier.urihttps://hdl.handle.net/20.500.12503/27701
dc.language.isoen
dc.provenance.legacyDownloads0
dc.titleArtemisinin Protects Oxidative Stress-induced Neuronal Apoptosis Via Up-Regulation of Akt/Bcl-2 Signaling
dc.typeposter
dc.type.materialtext

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