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目的初步探讨高迁移率族蛋白1(high mobility group protein B1,HMGB1)和肿瘤坏死因子α诱导蛋白3(tumor necrosis factorα-induced protein-3,TNFAIP3)在狼疮性肾炎(lupus nephritis,LN)患者和人类肾小球系膜细胞(human mesangial cell,HMC)增殖中的作用及机制。方法收集Ⅳ型LN患者的肾穿样本,采用免疫荧光和免疫组化技术检测肾小球细胞中HMGB1、TNFAIP3及IκBα蛋白表达水平;运用人重组HMGB1为刺激物刺激HMC,采用Brd U参入技术检测细胞增殖水平,并用Western blot技术检测TNFAIP3、IκBα及p65表达水平。结果与对照组相比,LN患者肾小球细胞中HMGB1及TNFAIP3蛋白表达升高,IκBα表达水平降低;体外实验证实,人重组HMGB1刺激HMC后,细胞增殖水平明显升高,同时在HMGB1刺激30 min后,与对照组相比,TNFAIP3的蛋白表达水平明显升高(P<0.05),而IκBα蛋白表达水平降低(P<0.05),随后p65蛋白表达明显升高(P<0.05)。结论 HMGB1和TNFAIP3可能通过活化NF-κB信号通路促进LN系膜细胞的过度增殖。
Objective To investigate the effects of high mobility group protein B1 (HMGB1) and tumor necrosis factor α-induced protein-3 (TNFAIP3) in patients with lupus nephritis (LN) The Role and Mechanism of Human Mesangial Cell Proliferation in Human. Methods Kidney-wearing samples from type IV LN patients were collected. The expression of HMGB1, TNFAIP3 and IκBα in glomerular cells were detected by immunofluorescence and immunohistochemistry. HMC was stimulated with human recombinant HMGB1 and BrdU incorporation assay The cell proliferation was detected by Western blot. The expression levels of TNFAIP3, IκBα and p65 were detected by Western blot. Results Compared with the control group, the expression of HMGB1 and TNFAIP3 in glomerular cells of LN patients increased and the expression of IκBα decreased. In vitro experiments showed that the proliferation of HMC was significantly increased after human recombinant HMGB1 stimulation, Compared with the control group, TNFAIP3 protein expression was significantly increased (P <0.05), while IκBα protein expression was decreased (P <0.05), and then p65 protein expression was significantly increased (P <0.05). Conclusion HMGB1 and TNFAIP3 may promote the proliferation of LN mesangial cells through activation of NF-κB signaling pathway.