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目的 :进一步明确白细胞介素 (IL 18)在肾组织免疫性损伤中的作用。方法 :应用半定量逆转录 多聚酶链反应(RT PCR)技术检测 16例正常人 ,16例原发性系膜增生性肾小球肾炎 (MsPGN)患者以及 18例狼疮性肾炎 (LN)患者外周血单个核细胞 (PBMC)白细胞介素 18受体 (IL 18R)α链mRNA的表达量 ,并用免疫组化方法检测 6例正常肾组织 ,16例MsPGN)患者及 18例LN患者肾组织IL 18Rα链蛋白表达量。结果 :MsPGN患者PBMCIL 18RmRNA表达量较正常组有所增高 ,但未达统计学意义 (P >0 0 5 ) ,LN患者PBMCIL 18RmRNA表达量较正常人显著增高 (P <0 0 0 1) ;正常肾组织存在较弱的IL 18R表达 ,MsPGN患者肾组织IL 18R表达量较正常肾组织有所增强 ,但未达统计学差异 ,而LN患者肾组织IL 18R的表达量较正常肾组及MsPGN组均显著增强 (P <0 0 0 1) ,但Pearson相关分析发现LN患者PBMC及肾组织IL 18R表达量均不与血清肌酐 (Scr)水平及 2 4小时尿蛋白排泌量 (2 4h UPE)存在相关关系。结论 :IL 18信号在全身系统及肾组织局部的免疫调节中起一定的作用 ;IL 18在肾功能未严重损害MsPGN患者的发病过程中可能所起作用不大 ;LN患者不但存在IL 18的过量产生 ,而且存在着IL 18过度作用的问题 ,抑制过强的IL 18作用信号可能是LN治疗的新途径。
Objective: To further clarify the role of interleukin (IL 18) in immune damage of renal tissue. Methods: The peripheral blood of 16 normal subjects, 16 patients with primary mesangial proliferative glomerulonephritis (MsPGN) and 18 patients with lupus nephritis (LN) were detected by semi-quantitative reverse transcriptase polymerase chain reaction (RT PCR) The expression of IL 18R alpha chain mRNA in mononuclear cells (PBMC) was detected by immunohistochemical method in 6 cases of normal kidney tissue and 16 cases of MsPGN and 18 cases of LN. Protein expression level. Results: The expression of PBMCIL 18R mRNA in MsPGN patients was higher than that in normal controls (P <0.05), and the expression of PBMCIL 18R mRNA in LN patients was significantly higher than that in normal controls (P <0.01) The expression of IL 18R in kidney tissue was weaker than that in normal kidney and MsPGN group, while the expression of IL 18R in kidney tissue of MsPGN group was higher than that of normal kidney tissue, but the difference was not statistically significant (P <0.01). However, Pearson correlation analysis showed that the expression of IL 18R in PBMCs and renal tissues of patients with LN was not related to the levels of serum creatinine (Scr) and 24 h urinary protein excretion (24 h UPE) There is a correlation. CONCLUSION: IL-18 signaling plays a role in the local immune regulation of systemic and renal tissues. IL 18 may not play a role in the pathogenesis of MsPGN, which is not seriously impaired in renal function. LN patients not only have excessive IL-18 And there is a problem of IL 18 over-action. Inhibition of excessive IL-18 signaling may be a new way of treating LN.