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

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

Research output: Contribution to journalArticle

6 Citations (Scopus)

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

Fingerprint

Glutamic Acid
Cell Death
artemisinine
Mitochondrial Membrane Potential
Antimalarials
Neuroprotective Agents
Reactive Oxygen Species
Oxidative Stress
Cardiovascular Diseases
Inflammation
Cell Line
Wounds and Injuries
Pharmaceutical Preparations
Neoplasms

Keywords

  • Akt
  • Apoptosis
  • Artemisinin
  • Neuroprotection
  • Oxidative stress

Cite this

@article{5629a47fd9bd4814b7232b472ec86eca,
title = "Artemisinin prevents glutamate-induced neuronal cell death via Akt pathway activation",
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",
author = "Lin, {Shao Peng} and Wenjun Li and Ali Winters and Ran Liu and Shaohua Yang",
year = "2018",
month = "4",
day = "20",
doi = "10.3389/fncel.2018.00108",
language = "English",
volume = "12",
journal = "Frontiers in Cellular Neuroscience",
issn = "1662-5102",
publisher = "Frontiers Media S.A.",

}

Artemisinin prevents glutamate-induced neuronal cell death via Akt pathway activation. / Lin, Shao Peng; Li, Wenjun; Winters, Ali; Liu, Ran; Yang, Shaohua.

In: Frontiers in Cellular Neuroscience, Vol. 12, 108, 20.04.2018.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Artemisinin prevents glutamate-induced neuronal cell death via Akt pathway activation

AU - Lin, Shao Peng

AU - Li, Wenjun

AU - Winters, Ali

AU - Liu, Ran

AU - Yang, Shaohua

PY - 2018/4/20

Y1 - 2018/4/20

N2 - 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.

AB - 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.

KW - Akt

KW - Apoptosis

KW - Artemisinin

KW - Neuroprotection

KW - Oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=85046786035&partnerID=8YFLogxK

U2 - 10.3389/fncel.2018.00108

DO - 10.3389/fncel.2018.00108

M3 - Article

AN - SCOPUS:85046786035

VL - 12

JO - Frontiers in Cellular Neuroscience

JF - Frontiers in Cellular Neuroscience

SN - 1662-5102

M1 - 108

ER -