17β-estradiol protects cortical neurons from ketamine-induced apoptosis
10.3969/j.issn.1001-1978.2014.06.017
- VernacularTitle:17β雌二醇对氯胺酮诱导皮层神经元凋亡的影响
- Author:
Jianli LI
;
Dongyan GAO
;
Yanru DU
;
Yanning HOU
- Publication Type:Journal Article
- Keywords:
17β-estradiol;
ketamine;
cortical neu-rons;
apoptosis;
Akt;
LY294002;
neuroprotection
- From:
Chinese Pharmacological Bulletin
2014;(6):816-820
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effects of 17β-es-tradiol on the apoptosis induced by ketamine in primary cultured cortical neurons. Methods Primary cultured cortical neurons were treated with different concentra-tions of ketamine or 17β-estradiol respectively. 24 hours after various treatments, neuron viability was measured by MTT assay. The structure of neurons was analyzed using microscope. Apoptotic neurons were de-termined by the TUNEL assay. The level of pAkt ex-pression was analyzed by Western blot. ResultsCompared with the control group, ketamine decreased neuron viability in a dose-dependent manner. Com-pared with ketamine group, 17β-estradiol increased neuron viability in a dose-dependent manner. Lack of three-dimensional sense,faded color,uncleared outline
were observed, and fractured neuron axons or neurons death were also observed in neurons treated by 100μmol · L-1 ketamine. 100 μmol · L-1 ketamine in-creased the number of apoptotic neurons and decreased the expression of pAkt. 0.1 μmol · L-1 17β-estradiol decreased the number of apoptotic neurons and in-creased the expression of pAkt. LY294002 inhibited the protective effects of 17β-estradiol, the number of apoptotic neurons increased, and the level of pAkt de-creased significantly. Conclusion 17β-estradiol ex-erts the neuroprotective effects against ketamine-in-duced neuroapoptosis by activating the PI3 K/Akt sig-naling pathway.
