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目的探讨白细胞介素６（ＩＬ－６）信号传递过程中某些成份（ＧＰ１３０、ＪｕｎＢ）在ＭｅｓＰＧＮ分子发病机制的作用。方法用原位杂交技术观察了ＭｅｓＰＧＮ患者肾活检组织肾小球细胞中ＩＬ－６、ＧＰ１３０、ＪｕｎＢｍＲＮＡ表达，并分析了其与患者肾小球系膜扩张、系膜细胞增殖程度、尿蛋白排泄量之间的关系。结果ＩＬ－６、ＧＰ１３０、ＪｕｎＢｍＲＮＡ表达分别是７．１±０．８、８．６±０．９、６．９±０．８，明显高于正常对照组（Ｐ＜０．０１），且相互间呈正相关；ＩＬ－６、ＧＰ１３０基因表达量与系膜扩张、尿蛋白排泄量呈正相关，中度系膜增殖性肾炎组、尿蛋白＞３．５克／日组，ＩＬ－６，ＧＰ１３０基因表达量明显高于轻度系膜增殖性肾炎组与尿蛋白＜３．５克／日组。结论ＩＬ－６及其信息传递中的ＧＰ１３０、ＪｕｎＢ基因异常表达在ＭｅｓＰＧＮ分子发病机制起一定作用。
Objective To investigate the role of GP130 and JunB in the pathogenesis of MesPGN during the signal transduction of interleukin-6 (IL-6). Methods The expression of IL-6, GP130 and JunB mRNA in glomerular cells of renal biopsies from patients with MesPGN was observed by in situ hybridization. The expressions of IL-6, GP130 and JunB mRNA in glomerular mesangial cells from patients with MesPGN were analyzed, and their relationship with glomerular mesangial expansion, mesangial cell proliferation, urinary protein excretion The relationship between. Results The expressions of IL-6, GP130 and JunB mRNA were 7.1 ± 0.8, 8.6 ± 0.9 and 6.9 ± 0.8, respectively, which were significantly higher than those in the normal control group (P <0.01) There was a positive correlation between IL-6, GP130 gene expression and mesangial dilation, urinary protein excretion was positively correlated with moderate mesangial proliferative glomerulonephritis group, urinary protein> 3.5 g / day group, IL-6, GP130 Gene expression was significantly higher than mild mesangial proliferative glomerulonephritis group and urinary protein <3.5 g / day group. Conclusion The abnormal expression of IL-6 and its signaling in GP130 and JunB plays a role in the pathogenesis of MesPGN.