Protective effect of 17β-estradiol against propofol-induced apoptosis of primarily cultured cortical neurons
10.16571/j.cnki.1008-8199.2015.09.006
- VernacularTitle:17β雌二醇对丙泊酚诱导原代培养皮层神经元凋亡的影响
- Author:
Jianli LI
;
Deyun YIN
;
Yunxin WANG
;
Xinxin PANG
;
Honghai WU
;
Yanning HOU
- Publication Type:Journal Article
- Keywords:
Propofol;
17β-estradiol;
neuroapoptosis;
Primarily cultured cortical neuron;
Mitochondrial membrane potential
- From:
Journal of Medical Postgraduates
2015;(9):925-928
- CountryChina
- Language:Chinese
-
Abstract:
Objective 17β-estradiol is known to have a neuroprotective effect.The aim of this study was to investigate the effects of 17β-estradiol on propofol-induced neuroapoptosis in primarily cultured cortical neurons. Methods Rat cortical neurons were primarily cultured for 7 days and randomly divided into groups A ( vehicle control) , B, and C, treated with equal volume of 20%intralipid, 500 μmol/L propofol, and 500 μmol/L propofol +0.1 μmol/L 17β-estradiol, respectively.At 12 hours after treatment, the morphology of the neurons was observed under the microscope, their survival rate calculated by MTT, their apoptosis was deter-mined by FCM assay, and their mitochondrial membrane potential measured by fluorescent dye rhodamine 123. Results Compared with group A, group B showed a significantly reduced number of neurons, lack of 3-dimensional appearance, unclear contour, and fractured neuron axons, but a remarkable improvement was observed in the propofol-induced morphological damage in group C.The survival rate of the neurons and the mitochondrial membrane potential were markedly decreased in group B ([52.3 ±5.2]% and [59.1 ± 5.3]%) as compared with groups A ( [99.9 ±3.6]%and [99.6 ± 5.8]%) and C ([90.1 ±7.2]%and [89.2 ±7.1]%) (both P<0.01 ) , while the rate of neuroapoptosis significantly increased in group B ([43.4 ±4.6]%) in comparison with A ([3.1 ±0.2]%) and C ([22.3 ±3.2]%) (both P<0.01). Conclusion 17β-es-tradiol can protect against propofol-induced apoptosis of primarily cul-tured neurons by inhibiting the reduction of their mitochondrial membrane potential.
