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机构地区:[1]第三军医大学新桥医院呼吸内科研究所,重庆400037
出 处:《中国现代医学杂志》2009年第16期2409-2412,2416,共5页China Journal of Modern Medicine
基 金:国家自然科学基金(30570808)
摘 要:目的研究核因子κB(NF-κB)抑制剂SN50对脂多糖(LPS)作用下小鼠巨噬细胞(Ana-1)炎性因子TNFαmRNA和蛋白表达的影响及其对NF-κBp65亚基核移位的抑制作用。方法用MTT法检测SN50对细胞增殖活性的影响,行RT-PCR和ELISA法检测巨噬细胞经LPS作用和SN50处理后TNFαm-RNA和蛋白表达变化,用Western-Blot检测NF-κBp65亚基核移位情况。结果在LPS作用下炎性因子TNFα强烈升高,并呈现时间依赖性,SN50干预后可明显抑制NF-κBp65亚基核移位和TNFα表达,其中以早期使用SN50效果最佳。结论SN50可以通过抑制NF-κBp65亚基核移位来降低LPS作用下巨噬细胞的TNFα的产生。[ Objective ] To investigate the effect of SN50, an inhibitor of nuclear factor κB (NF-κB), on the TNFα production and on the activity of NF-κB in the mouse maerophage (Ana-1) stimulated by LPS. [Methods] Ana-1 cell's proliferation affected by SN50 was measured by MTT. The TNFot mRNA level was assayed by RT-PCR and the production of protein was measured by ELISA after being activated by LPS and being treated by SN50. The activity of NF-κB was assayed by Western-Blot. [ Results ] SN50 inhibited LPS-stimulated mRNA expression and production of TNFα in a eoneentration-dependent manner, as well as the activity of NF-κ. SN50 would do better if it was used as early as it could. [ Conclusion ] The inhibitory effect of SN50 on the production of TNFα in LPS- stimulated Ana-1 may be mediated by suppression of NF-κB activity.
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