同型半胱氨酸硫内酯-内质网应激途径促进HUVECs黏附  

Homocysteine thiolactone-endoplasmic reticulum stress pathway promotes HUVECs adhesion

作　　者：黄宁江[1] 黄海 姜卓 黄仕芳 胡昊良 HUANG Ning-jiang;HUANG Hai;JIANG Zhuo;HUANG Shi-fang;HU Hao-liang(Dept.of Pharmacology,Yongzhou Vocational Technical College,Yongzhou 425000;the First Hospital of Yongzhou Yongzhou 425000;College of Life Sciences,Hunan Normal University,Changsha 410081,China)

机构地区：[1]永州职业技术学院药学系,湖南永州425000 [2]永州市第一人民医院,湖南永州425000 [3]湖南师范大学生命科学学院,湖南长沙410081

出　　处：《基础医学与临床》2018年第9期1274-1279,共6页Basic and Clinical Medicine

基　　金：湖南省教育厅科研项目(17C1608)

摘　　要：目的探讨同型半胱氨酸硫内酯(HTL)通过内质网应激途径促人脐静脉内皮细胞(HUVECs)黏附的可能机制。方法取HTL处理的大鼠胸主动脉,检测NF-κB p65的表达;用Western blot检测HUVECs中HTL,分别对其进行时效与量效处理后,所谓检测内质网应激蛋白Bip和Chop及黏附蛋白VCAM-1和ICAM-1的表达,以及内质网应激激动剂与抑制剂对HTL诱导的HUVECs黏附因子表达的影响;用"STRING"预测Bip(HSPA5)和Chop(DDIT3)与黏附因子VCAM-1和ICAM-1的相互作用。结果 HTL诱导大鼠胸主动脉血管的内皮细胞NF-κB p65表达,促HUVECs的内质网应激蛋白Bip和Chop及黏附因子VCAM-1和ICAM-1的表达(P<0.05),内质网激动剂上调HTL对黏附因子的表达,内质网抑制剂抑制HTL对黏附因子的表达(P<0.05);"STRING"软件预测内质网应激蛋白Bip和Chop与黏附因子VCAM-1和ICAM-1具有相互作用。结论 HTL可能通过内质网应激途径促进HUVECs黏附。Objective To investigate the potential mechanisms that homocysteine thiolactone（ HTL） promotes human umbilical vein endothelial cells（ HUVECs） via endoplasmic reticulum stress pathway. Methods To detect the expression of NF-κB p65 in rat thoracic aortic dissection tissue treated by HTL. Culturing HUVECs,dealing with HTL by a time dependent and does dependent manner. We detected the expression of endoplasmic reticulum stress protein Bip and Chop. Meanwhile we detected the expression of adhesive protein VCAM-1 and ICAM-1. Using the endoplasmic reticulum stress agonist and inhibitor deal with HUVEC,respectively. Then detected the affection of endoplasmic reticulum stress agonist and inhibitor on the expression of the adhesive protein in HUVECs induced by HTL,respectively. Using the protein interaction prediction tool ＂STRING＂predicted the interaction between endoplasmic reticulum stress protein and adhesive protein. Results HTL induced the endothelial injury in isolated vessels; HTL increased the expressions of endoplasmic reticulum stress protein Bip and Chop in HUVECs（ P〈0. 05）; HTL upregulated the expressions of adhesive protein VCAM-1 and ICAM-1 in HUVECs（ P〈0. 05）; Endoplasmic reticulum stress agonist promote the expression of adhesive protein VCAM-1 and ICAM-1 in HUVECs（ P〈0. 05）; Endoplasmic reticulum stress inhibitor downregulated the expression of adhesive protein VCAM-1 and ICAM-1 in HUVECs（ P〈0. 05）; The protein interaction prediction tool ＂STRING ＂predicted the endoplasmic reticulum stress protein and adhesive protein had interactions. Conclusions HTL may promote endothelial cell adhesion via endoplasmic reticulum stress pathway.

关 键 词：同型半胱氨酸硫内酯 内质网应激 黏附因子 内皮黏附 

分 类 号：R318.11[医药卫生—生物医学工程]