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[Osthole ameliorates glutamate-induced toxicity in HT22 cells via activating PI3K/Akt signaling pathway]
Xiaoyuan Mao1, Zhibin Wang1, Honghao Zhou1
1Institute of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008; Institute of Clinical Pharmacology; Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha 410078, China.
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.
