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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 effects of SN50, an inhibitor of nuclear factor κB (NF-κB), on the expression of TNFα mRNA and protein in mouse macrophages (Ana-1) induced by lipopolysaccharide (LPS) and its effect on nuclear translocation of NF-κBp65 Inhibition of the position. Methods MTT assay was used to detect the effect of SN50 on cell proliferation. The expression of TNFαmRNA and protein in macrophages treated with LPS and SN50 was detected by RT-PCR and ELISA. The NF-κBp65 subunit Shift situation. Results Under the action of LPS, the inflammatory factor TNFα was strongly and time-dependent. SN50 could significantly inhibit the subunit nuclear translocation and TNFα expression of NF-κB p65, and SN50 was the best. Conclusion SN50 can reduce the production of TNFα by macrophages by inhibiting subunit NF-κBp65 translocation.