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目的 研究核因子ＫＢ（ＮＦ－ＫＢ）在氧化低密度脂蛋白（Ｏｘ- ＬＤＬ）诱导的体外培养的人肾小球系膜细胞表达单核／巨噬细胞趋化蛋白－１（ＭＣＰ－１）中的作用。方法 采用凝胶迁移率变动分析检测ＮＦ－ＫＢ的ＤＮＡ结合活性变化，以免疫组织化学观测细胞内ｐ６５的核转位，用细胞ＥＬＩＳＡ法检测细胞内 ＭＣＰ－１及ＩＫＢα蛋白含量变化。结果 不同浓度（１０、２５、５０、１００μｇ／ｍｌ）Ｏｘ－ＬＤＬ刺激肾小球系膜细胞均可引起细胞ＮＦ-ＫＢ的ＤＮＡ结合活性增强、ＩＫＢα蛋白表达下降以及ＭＣＰ－１蛋白表达增强，以５０μｇ／ｍｌ刺激１ｈ ＮＦ－ＫＢ活化及ＩＫＢα表达减弱最明显，作用２４ｈＭＣＰ-１表达水平最高。ＮＦ－ＫＢ俯活化的同时伴有ｐ６５核转位。上述效应可被ＮＦ－ＫＢ特异性抑制剂吡咯二硫氨基甲酸酯（ＰＤＴＣ）所抑制。结论Ｏｘ－ＬＤＬ刺激人肾小球系膜细胞产生ＭＣＰ－１是由ＮＦ－ＫＢ调控，ＮＦ－ＫＢ参与了脂质肾损害的发病过程。
Objective To investigate the effect of nuclear factor KB (NF-KB) on the expression of monocyte chemoattractant protein-1 (MCP-1) in cultured human glomerular mesangial cells induced by Oxidized Low Density Lipoprotein (Ox-LDL) In the role. Methods The change of DNA binding activity of NF-KB was detected by gel mobility shift assay. The intracellular p65 nuclear translocation was detected by immunohistochemistry. The intracellular protein content of MCP-1 and IKBα was detected by ELISA. Results Oxidized LDL at different concentrations (10, 25, 50 and 100μg / ml) stimulated the mesangial cells to increase the DNA-binding activity of NF-KB, decrease the expression of IKBα and enhance the expression of MCP- The activation of NF-KB and the reduction of IKBα expression at 50μg / ml for 1h were the most obvious, and the expression of MMP-1 was the highest at 24h. NF-KB inactivation accompanied by p65 nuclear translocation. The above effects can be inhibited by pyrrolodithiocarbamate (PDTC), a specific inhibitor of NF-KB. Conclusion Ox-LDL stimulates the production of MCP-1 in human mesangial cells by NF-KB, which is involved in the pathogenesis of lipid-induced renal damage.