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作 者:罗海波[1] 吕爱贞 卢晓[2] 富宁[2] 吴砂[2] 郑华[3]
机构地区:[1]广州军区解放军第421医院检验输血科,广州510310 [2]南方医科大学基础医学院免疫学教研室,广州510515 [3]南方医科大学南方医院心内科,广州510515
出 处:《重庆医学》2014年第5期575-577,581,共4页Chongqing medicine
基 金:国家自然基金资助项目(30901341)
摘 要: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4d后,Toll样受体4(TLR4)激动剂脂多糖(LPS)刺激24h,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NF-κB通路的活化(P<0.05)。而经过DX预处理的Raw264.7,镍钛合金促进Raw264.7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NTS抑制Raw264.7细胞对TLR4激动剂LPS的免疫应答。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 .
分 类 号:R541.4[医药卫生—心血管疾病]
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