Osthole ameliorates glutamate-induced toxicity in HT22 cells via activating PI3K/Akt signaling pathway / 中南大学学报(医学版)
Journal of Central South University(Medical Sciences)
;
(12): 955-959, 2015.
Article
in Chinese
| WPRIM
| ID: wpr-815243
ABSTRACT
OBJECTIVE@#To investigate the neuroprotective effects of osthole (OST) on glutamate-induced toxicity in hippocampal HT22 cells and to explore the correlation between the protection and phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) signaling pathway.
@*METHODS@#The cell injury model of HT22 was induced by glutamate and the cell viability was detected by MTS assay. The lactate dehydrogenase (LDH) release and the caspase-3 activity were determined by commercial kits. Western blot analysis was utilized to detect the protein levels of PI3K, Akt, p-PI3K and p-Akt.
@*RESULTS@#OST markedly improved the cell survival and decreased the LDH release in glutamate-treated HT22 cells in a dose-dependent manner. Furthermore, the levels of p-PI3K and p-Akt proteins were significantly increased in glutamate and OST-co-treated HT22 cells. The effect of OST on p-Akt phosphorylation in HT22 cells was attenuated in the presence of PI3K specific inhibitor (LY294002).
@*CONCLUSION@#OST protects HT22 cells from glutamate excitotoxicity through a mechanism involving the activation of PI3K/Akt signaling pathway.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Phosphorylation
/
Signal Transduction
/
Cell Line
/
Cell Survival
/
Morpholines
/
Chromones
/
Neuroprotective Agents
/
Glutamic Acid
/
Phosphatidylinositol 3-Kinases
Limits:
Animals
Language:
Chinese
Journal:
Journal of Central South University(Medical Sciences)
Year:
2015
Type:
Article
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