Effects of 17β-estradiol on Ketamine-induced Neuroapoptosis
10.3870/yydb.2014.11.009
- VernacularTitle:17β雌二醇对氯胺酮所致神经元凋亡的影响
- Author:
Jianli LI
;
Wei LIANG
;
Honghai WU
;
Yanning HOU
- Publication Type:Journal Article
- Keywords:
17β-estradiol;
Ketamine;
Cortex neurons;
Neuroa apoptosis
- From:
Herald of Medicine
2014;(11):1434-1438
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect and the mechanisms of 17β-estradiol on ketamine-induced apoptosis on primary cultured rat cortical neurons. Methods Cortical neurons were primarily cultured for seven days,then divided into four groups :control group ( treated with equal valume of DMSO ),estradiol-treated group ( treated with 0.1 μmol·L-1 17β-estradiol),ketamine-treated group(treated with 100 μmol·L-1 ketamine),ketamine plus 17β-estradiol-treated group( treated with 0. 1 μmol·L-1 17β-estradiol+100μmol·L-1 ketamine). The neurons were treated for 24 hours. The neuron viability was determined by MTT. Neuroapoptosis was measured by nuclear morphometry after Hoechest 33258 dying. Western blotting was performed to detect the expression levels of cleaved-caspase-3 and Bcl-2protein. Results The neuron viability in the ketamine group was(54. 02±7. 78)%,significantly decreased from the control group,whereas ketamine plus 17β-estradiol increased the cell viability to(88. 09±6. 54)%,significantly higher than the ketamine group. The neuroapoptosis rate in the ketamine group was(49. 50±4. 34)%,significantly increased from the control group,while that in the drug combination group was(15. 74 ± 3. 40)%,significantly lower compared with the ketamine group. Meanwhile,the cleaved-caspase-3 expression increased,and Bcl-2 expression decreased remarkably after ketamine treatment,while which was reversed in the drug combination group. Conclusion 17β-estradiol can protect against ketamine-induced injury by inhibiting neuron apoptosis.
