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目的 探讨核因子 κB(NF κB)活化在肾小球肾炎发病机制中的作用及糖皮质激素对NF κB活化的调节作用。方法 肾毒血清肾炎应用兔抗鼠肾小球基底膜肾毒血清制备。模型组 :注射肾毒血清后不加任何治疗 ,第 14d处死 ;糖皮质激素干预组 (治疗组 ) :于肾毒血清注射后第 1～ 14d给予地塞米松每日 0 .12 5mg/kg腹腔注射。采用免疫组化及医学图像分析系统观察肾小球及肾小管中NF κB活化和单核细胞趋化蛋白 1(MCP 1)的表达 ,并分析其与蛋白尿和肾小球细胞数之间的关系。结果 模型组肾小球及肾小管中NF κB活化较正常对照组显著上调 ,分别为 (38.2 7± 8.83) %vs (1.82± 0 .6 8) %和 (6 8.46± 12 .94) %vs (16 .89± 4.47) % ,P均 <0 .0 1;模型组肾小球及肾小管中MCP 1表达分别为 (2 4.37± 7.0 6 )个 / gcs和 (5 4.78± 11.49) % ,较正常对照组显著升高(P <0 .0 1) ,肾小球中NF κB活化和MCP 1表达与单核细胞浸润和蛋白尿密切相关 ;糖皮质激素干预组肾小球及肾小管中NF κB活化和MCP 1表达均显著下调。结论 NF κB活化在肾小球肾炎发病机制中发挥重要作用 ,抑制NF -κB活化可能是糖皮质激素抗肾炎作用的机制之一。
Objective To investigate the role of nuclear factor κB (NF κB) activation in the pathogenesis of glomerulonephritis and the regulation of NF κB activation by glucocorticoids. Methods Nephrotoxic serum nephritis rabbit anti-rat glomerular basement membrane nephrotoxic serum preparation. The model group was treated with nephrotoxic serum without any treatment and then sacrificed on the 14th day. Glucocorticoid intervention group (treatment group): dexamethasone was administered daily at 0.12 mg / kg to 5 mg / kg on days 1 to 14 after nephrotoxic injection injection. Immunohistochemistry and medical image analysis system were used to observe the expression of NF κB activation and monocyte chemotactic protein 1 (MCP 1) in glomeruli and tubules, and to analyze the relationship between proteinuria and glomerular cell number relationship. Results The activation of NF-κB in glomeruli and tubules in model group was significantly higher than that in normal control group (38.2 7 ± 8.83)% vs (1.82 ± 0.68%) and (6 8.46 ± 12.94)% vs (16.89 ± 4.47)% and P <0.01 respectively. The expression of MCP 1 in glomeruli and tubules in model group were (2.43.7 ± 7.06) / gcs and (4.78 ± 11.49)%, respectively (P <0.01). The activation of NF-κB and the expression of MCP-1 in glomerulus were closely related to the infiltration of mononuclear cells and proteinuria. In the glucocorticoid intervention group, glomerular and tubular NFκB activation and MCP 1 expression were significantly down-regulated. Conclusion NF κB activation plays an important role in the pathogenesis of glomerulonephritis. Inhibition of NF-κB activation may be one of the mechanisms of glucocorticoid-anti-nephritis effect.