Epidermal growth factor treatment has protective effects on the integrity of the blood-brain barrier against cerebral ischemia injury in bEnd3 cells

被引:18
作者
Yang, Shu [1 ]
Jin, Hong [2 ]
Zhao, Zhi-Gang [1 ]
机构
[1] Capital Med Univ, Beijing Tiantan Hosp, Dept Pharm, 119 Nansihuan Xilu Rd, Beijing 100070, Peoples R China
[2] Inst Dis Prevent & Control PLA, Disinfect Evaluat Res Ctr, Beijing 100071, Peoples R China
基金
中国国家自然科学基金;
关键词
epidermal growth factor; blood-brain barrier; ischemia; tight junctions; bEnd3; OXYGEN GLUCOSE DEPRIVATION; IN-VITRO; REPERFUSION INJURY; ENDOTHELIAL-CELLS; EXPRESSION; PERMEABILITY; DISRUPTION; OCCLUDIN; INVOLVEMENT; DELIVERY;
D O I
10.3892/etm.2019.7186
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Tight junctions (TJs) serve an important role in maintaining the integrity of the blood-brain barrier (BBB), while neurological disorders, including ischemic stroke, induce TJ disruption and increase BBB permeability; results include edema formation and hemorrhage transformation. Cerebral endothelium protection presents a promising approach in ischemic stroke therapy. In the current study, protective effects of the epidermal growth factor (EGF) on ischemia-induced disruption of BBB integrity were examined using an oxygen-glucose deprivation (OGD) model in bEnd3 cells. Expression levels of claudin-5 and TJ protein-1 (ZO-1) were determined by reverse transcription-quantitative polymerase chain reaction and western blot analysis. Cell viability was evaluated by cell counting kit-8 assay and the endothelial permeability of Lucifer yellow (LY) was assessed using Transwell assays. The results revealed that post-ischemia administration of EGF (250 ng/ml) significantly attenuated the decrease in mRNA (P<0.05) and protein (P<0.01) expression levels of claudin-5 and ZO-1, and the increase in endothelial permeability of LY (P<0.05) induced by 4 h OGD exposure followed by 24 h reoxygenation. In addition, EGF did not significant affect cell viability. The current study suggested a potential of EGF to improve BBB integrity against ischemic injury by upregulating the expression of TJ proteins and reducing endothelial permeability.
引用
收藏
页码:2397 / 2402
页数:6
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