Hypoxia/Aglycemia-induced endothelial barrier dysfunction and tight junction protein downregulation can be ameliorated by citicoline.
Hypoxia/Aglycemia-induced endothelial barrier dysfunction and tight junction protein downregulation can be ameliorated by citicoline.
复制标题
胞二磷胆碱可以改善缺氧/血糖引起的内皮屏障功能障碍和紧密连接蛋白下调
DOI：
10.1371/journal.pone.0082604
复制
发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Chen Y
中科院分区：
文献类型：
--
作者：
Ma X;Zhang H;Pan Q;Zhao Y;Chen J;Zhao B;Chen Y
本研究探讨胞二磷胆碱对内皮细胞在低氧/高血糖条件下通透性和紧密连接蛋白(TJPs)表达的影响。采用低氧或缺氧缺糖(OGD)诱导人脐静脉内皮细胞(HUVECs)和小鼠脑微血管内皮细胞(bEnd.3s)内皮屏障破坏模型。测定胞二磷胆碱在低浓度和高浓度下对内皮细胞屏障破坏模型的影响。用FITC-葡聚糖流量计检测内皮通透性。用免疫荧光、实时定量聚合酶链式反应和Western Blot方法检测TJPs的表达。结果表明，缺氧或OGD使HUVECs通透性增加，同时在mRNA和蛋白水平下调了occludens-1(ZO-1)和occludin的表达。同样，在bEnd.3S中，缺氧增加了通透性，降低了ZO-1和claudin-5的表达。胞二磷胆碱治疗可剂量依赖性地降低这两种模型的通透性，这与TJPs的表达升高是平行的。结果表明胞二磷胆碱可能通过上调TJPs的表达来恢复缺氧/高血糖损伤的内皮细胞的屏障功能。
This study explores the effect of citicoline on the permeability and expression of tight junction proteins (TJPs) in endothelial cells under hypoxia/aglycemia conditions. Hypoxia or oxygen and glucose deprivation (OGD) was utilized to induce endothelial barrier breakdown model on human umbilical vein endothelial cells (HUVECs) and mouse brain microvascular endothelial cells (bEnd.3s). The effect of citicoline on endothelial barrier breakdown models was determined at either low or high concentrations. FITC-Dextran flux was used to examine the endothelial permeability. The expression of TJPs was measured by immunofluorescence, Real-time PCR and Western Blot methods. Results showed that hypoxia or OGD increased the permeability of HUVECs accompanied with down-regulation of occludens-1 (ZO-1) and occludin at both mRNA and protein levels. Similarly in bEnd.3s, hypoxia increased the permeability and decreased the expression of ZO-1 and claudin-5. Citicoline treatment dose-dependently decreased the permeability in these two models, which paralleled with elevated expression of TJPs. The data demonstrate that citicoline restores the barrier function of endothelial cells compromised by hypoxia/aglycemia probably via up-regulating the expression of TJPs.
登录
查看更多内容
影响因子：
3.7
作者：
Huang SH;Wang L;Chi F;Wu CH;Cao H;Zhang A;Jong A
通讯作者：
Jong A
影响因子：
6
作者：
Koto, Takashi;Takubo, Keiyo;Ikeda, Eiji
通讯作者：
Ikeda, Eiji
影响因子：
3.1
作者：
Ilcol, Yesim Ozarda;Yilmaz, Zeki;Ulus, Ismail H.
通讯作者：
Ulus, Ismail H.
影响因子：
6.1
作者：
Hurtado, O;Moro, MA;Lizasoain, I
通讯作者：
Lizasoain, I
影响因子：
3.7
作者：
Rajadas J;Sun W;Li H;Inayathullah M;Cereghetti D;Tan A;de Mello Coelho V;Chrest FJ;Kusiak JW;Smith WW;Taub D;Wu JC;Rifkind JM
通讯作者：
Rifkind JM