IL-1βstimulated neuron activation via PI3K/Akt/mTOR pathway
10.3969/j.issn.1000-4718.2015.03.003
- VernacularTitle:IL-1β通过 PI3K／Akt／mTOR 途径促进神经元活化
- Author:
Na GAN
;
Fei YIN
;
Jing PENG
;
Liwen WU
;
Fang HE
;
Chen CHEN
- Publication Type:Journal Article
- Keywords:
Interleukin-1β;
Mammalian target of rapamycin;
Medial temporal lobe epilepsy;
Neuron activation
- From:
Chinese Journal of Pathophysiology
2015;(3):397-402
- CountryChina
- Language:Chinese
-
Abstract:
[ ABSTRACT] AIM:To study the effect of interleukin-1β( IL-1β) on neuron activation during the process of me-dial temporal lobe epilepsy ( MTLE ) .METHODS: IL-1β, rapamycin [ an inhibitor of mammalian target of rapamycin (mTOR)]and lentiviral transfection to knockdown PI3K-p85 were used to pre-treat the neurons.The protein levels of PI3K-p85, p-Akt, p-p70S6K and MAP2 were detected and the relationship among the tested cytokines was analyzed.The neuron endocytosis was observed in each group.RESULTS:IL-1βincreased the protein levels of PI3K-p85, p-Akt and p-p70S6K, up-regulated the expression of PI3K-p85 binding with IL-1RI in the neurons, and increased the neuron endocyto-sis compared with control group (P<0.05) .These processes were inhibited by rapamycin and silence of PI3K-p85 (P<0.05).Inhibition of the PI3K-p85 binding to IL-1RI decreased the protein levels of p-Akt, p-p70S6K and MAP2 which were increased by IL-1βstimulation (P<0.05).CONCLUSION: IL-1βactivates PI3K-p85 by binding with IL-1RI to promote the activation and proliferation of neuron synapses via PI3K/Akt/mTOR signaling pathway, which might be one of the mechanisms in MTLE chronic progress.
