CAJ | 학술논문

目的：研究镍钛合金心血管支架（NTS）及地塞米松（DX）抗支架过敏治疗对单核巨噬细胞革兰阴性菌脂多糖（LPS）刺激的影响。方法单核巨噬细胞系Raw264．7细胞组与DX预处理Raw264．7细胞组，NTS作用4 d后，Toll样受体4（TLR4）激动剂脂多糖（LPS）刺激24 h ，流式细胞术检测细胞表面标志CD80、CD86、FasL等分子表达；ELISA检测培养液促炎症因子IL-6、TNF-α；特异荧光素酶试剂盒检测 NF-κB、干扰素-γ序列（GAS）、干扰素刺激反应元件（ISRE）、信号转导与转录活化因子3（STAT3）细胞炎症因子相关信号通路的活化。结果镍钛合金作用后，促进LPS介导的Raw264．7细胞表达CD80分子，抑制其表达FasL ，降低IL-6分泌，抑制细胞内N F-κB通路的活化（ P＜0．05）。而经过DX预处理的Raw 264．7，镍钛合金促进Raw 264．7细胞表达CD80、FasL分子，增加TNF-α分泌，抑制胞内炎症信号通路NF-κB、ISRE、STAT3等通路的活化（P＜0．05）。结论N T S抑制Raw 264．7细胞对T L R4激动剂L PS的免疫应答。
목적：연구얼태합금심혈관지가（NTS）급지새미송（DX）항지가과민치료대단핵거서세포혁란음성균지다당（LPS）자격적영향。방법단핵거서세포계Raw264．7세포조여DX예처리Raw264．7세포조，NTS작용4 d후，Toll양수체4（TLR4）격동제지다당（LPS）자격24 h ，류식세포술검측세포표면표지CD80、CD86、FasL등분자표체；ELISA검측배양액촉염증인자IL-6、TNF-α；특이형광소매시제합검측 NF-κB、간우소-γ서렬（GAS）、간우소자격반응원건（ISRE）、신호전도여전록활화인자3（STAT3）세포염증인자상관신호통로적활화。결과얼태합금작용후，촉진LPS개도적Raw264．7세포표체CD80분자，억제기표체FasL ，강저IL-6분비，억제세포내N F-κB통로적활화（ P＜0．05）。이경과DX예처리적Raw 264．7，얼태합금촉진Raw 264．7세포표체CD80、FasL분자，증가TNF-α분비，억제포내염증신호통로NF-κB、ISRE、STAT3등통로적활화（P＜0．05）。결론N T S억제Raw 264．7세포대T L R4격동제L PS적면역응답。
Objective To study the effect of nickel-titanium stent(NTS) and consequent anti-allergy dexamethasone therapy on macrophage cells reactivity to lipopolysaccharide (LPS) from gram-negative bacterium .Methods The macrophage cell line Raw 264 .7 and dexamethasone-pretreated Raw264 .7 were co-cultured with NTS for 4 days ,and stimulated with LPS for 24 hours .The surface marker CD molecules of CD80 ,CD86 and FasL were detected with flowcytometr method ,the supernant cytokine production of proinflammatory cytokines IL-6 and TNF-αwas valued with ELISA method ,and intracellular inflammatory signal pathway acti-vation of NF-κB ,GAS ,ISRE and STAT3 was checked with signal molecule specific promoter lunciferase analysis .Results The stent pre-treatment improved LPS-mediated CD80 expression ,suppressed FasL production ,decreased IL-6 secretion and NF-κB ac-tivation ,the results have statistical significance (P<0 .05) .The dexamethasone treatment improved stent-mediated up-regulated ex-pression of CD80 ,FasL and TNF-α,and suppressed the activation of intracellular inflammatory signal pathway of NF-κB ,ISRE and STAT3 ,the results have statistical significance(P<0 .05) .Conclusion NTS inhibit macrophage cells Raw264 .7 react to TLR4 ag-onist LPS ,and dexamethasone treatment improved the function .