p38/ATF-2通路参与C反应蛋白诱导的内皮细胞活化  

p38 MAPK/ATF-2 pathway is involved in C-relative protein-induced endothelial cell activation

作　　者：刘少军[1] 李沅美 刘慰华[1] 熊龙根[1] 刘世明[1] 

机构地区：[1]广州医科大学附属第二医院广州心血管疾病研究所/心内科,广东广州510260 [2]广东药学院生命科学与生物制药学院,广东广州510006

出　　处：《中国病理生理杂志》2015年第5期808-811,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81300151);广东省自然科学基金重点项目(No.S2011020002143)

摘　　要：目的：考察p38 MAPK／ATF-2通路在C反应蛋白（ CRP）诱导的内皮细胞活化中的作用。方法：采用培养的人冠状动脉内皮细胞（ HCAEC）第3～7代用于实验。 CRP刺激诱导内皮细胞活化，给予p38抑制剂SB203580和SB202190干预。免疫印迹法检测p-eNOS、p-p38和p-ATF2的水平；ELISA法测定HCAEC分泌的黏附分子ICAM-1、VCAM-1和MCP-1的变化。结果： CRP呈浓度依赖性地抑制p-eNOS水平， CRP诱导HCAEC分泌ICAM-1、VCAM-1和MCP-1；CRP激活p38／ATF-2通路；SB203580和SB202190部分恢复p-eNOS水平和抑制CRP诱导的ICAM-1、VCAM-1和MCP-1分泌。结论：p38 MAPK／ATF-2通路参与CRP诱导的HCAEC活化。AIM：To investigate the role of p38 MAPK/ATF-2 pathway in C-relative protein （ CRP）-induced endothelial cell activation.METHODS：Human coronary artery endothelial cells （ HCAEC） were cultured and were used between passages 3 and 7.CRP served as a stimulus for endothelial cell activation.Western blotting was performed to de-termine the expression and phosphorylation of eNOS, p38 and ATF2.ELISA was carried out to detect the levels of ICAM-1, VCAM-1 and MCP-1 released from HCAEC.Pharmacological p38 inhibitors SB203580 and SB202190 were used to de-termine the effect of p38/ATF-2 pathway.RESULTS：CRP reduced the p-eNOS level in a concentration-dependent man-ner and induced the release of ICAM-1, VCAM-1 and MCP-1.The p38/ATF-2 pathway was activated by CRP treatment. SB203580 and SB202190 partially rescued p-eNOS level and suppressed the secretion of ICAM-1, VCAM-1 and MCP-1. CONCLUSION：p38MAPK/ATF-2 pathway participates in CRP-induced endothelial activation.

关 键 词：P38 MAPK/ATF-2通路 C反应蛋白 内皮细胞活化 动脉粥样硬化 

分 类 号：R541[医药卫生—心血管疾病]