CAJ | 학술논문

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。
목적：고찰p38 MAPK／ATF-2통로재C반응단백（ CRP）유도적내피세포활화중적작용。방법：채용배양적인관상동맥내피세포（ HCAEC）제3～7대용우실험。 CRP자격유도내피세포활화，급여p38억제제SB203580화SB202190간예。면역인적법검측p-eNOS、p-p38화p-ATF2적수평；ELISA법측정HCAEC분비적점부분자ICAM-1、VCAM-1화MCP-1적변화。결과： CRP정농도의뢰성지억제p-eNOS수평， CRP유도HCAEC분비ICAM-1、VCAM-1화MCP-1；CRP격활p38／ATF-2통로；SB203580화SB202190부분회복p-eNOS수평화억제CRP유도적ICAM-1、VCAM-1화MCP-1분비。결론：p38 MAPK／ATF-2통로삼여CRP유도적HCAEC활화。
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.