Effect of 14,15-EET on Release of BDNF from Astrocytes and Neuronal Apoptosis in a Co-culture System after Oxygen-glucose Deprivation and Reperfusion
10.3870/j.issn.1672-0741.2019.04.001
- VernacularTitle:14,15-EET对氧糖剥夺/再灌注模型中星形胶质细胞分泌BDNF及共培养体系中神经元凋亡的影响
- Author:
Zuofan Li
1
;
Chuanhan Zhang
1
;
Li Wan
1
Author Information
1. Department of Anesthesiology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China
- Publication Type:Journal Article
- Keywords:
oxygen-glucose deprivation;
astrocytes;
neurons;
14,15-epoxyeicosatrienoic acids;
brain derived neurotrophic factor
- From:
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
2019;48(4):377-381
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate whether post-treatment of cultured astrocytes with 14,15-epoxyeicosatrienoic acids（14,15-EET）would increase the brain derived neurotrophic factor（BDNF）secretion after oxygen-glucose deprivation and reperfusion（OGD/R）, and if this effect would subsequently protect neurons during reperfusion after OGD in the co-cultured system.
Methods:Astrocytes and neurons were subjected to OGD/R. Exogenous 14,15-EET were applied to astrocytes in the reperfusion period and ELISA was then performed to measure BDNF secretion from astrocytes at different time points following OGD/R. After that，the OGD neurons were co-cultured with the astrocytes that were previously incubated with DMSO or 14,15-EET.Tunnel staining was used to detect neuronal apoptosis.
Results:BDNF secretion was significantly promoted by application of 14,15-EET on astrocytes in the reperfusion stage after OGD. Exposure of OGD neurons to astrocyte media previously conditioned with 14,15-EET reduced the neuronal apoptosis，but the pro-survival effect could be partly reversed by TrkB inhibitor k252a.
Conclusion:Exogenous administration of 14,15-EET augments BDNF secretion from astrocytes，which increases TrkB receptor occupancy on neurons and promotes neuronal survival after OGD/R.
