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为了探讨白细胞介素 18(IL 18)在狼疮性肾炎 (LN )发生、发展中的作用。我们采用逆转录多聚酶链反应 (RT PCR )及酶联免疫吸附 (ELISA )法测定 16例正常人及 18例LN患者外周血单个核细胞 (PBMC )IL 18mRNA表达量及其血浆水平。结果提示LN患者PBMCIL 18mRNA表达量及血浆IL 18水平均较正常对照组显著增高 [IL 18mRNA表达量为 :1 2 6 2± 0 189vs0 84 4± 0 15 5 ,P <0 0 0 1;IL 18血浆水平为 :(82 2 0 9± 5 32 77)pg/mlvs (2 39 5 7± 75 0 6 )pg/ml,P <0 0 0 1]。且WHOIV型LN增高较非IV型LN更为显著 [IL 18mRNA表达量为 :1 32 9± 0 2 1vs 1 138± 0 15 2 3,P <0 0 5 ;IL 18血浆水平为 :(1135 5 4± 5 15 34)pg/mlvs (5 0 8 6 5± 341 36 )pg/ml,P <0 0 1]。另外 ,血浆IL 18水平与肾组织活动指数 ,肾小管间质损害程度呈等级相关 (r分别为 :0 6 10和 0 4 99,P均 <0 0 5 ) ,也与血清肌酐 (Scr) ,血清内生肌酐清除率 (Ccr)及 2 4h尿蛋白排泄量 (2 4hUPQ )呈直线相关 (r分别为 :0 898、 0 6 2 8和 0 5 37,P均 <0 0 5 )。本研究认为循环IL 18表达和分泌增高可能参与LN的免疫发病过程 ,并与狼疮活动有一定的关系
To explore the role of interleukin 18 (IL 18) in the development and progression of lupus nephritis (LN). We used reverse transcription polymerase chain reaction (RT PCR) and enzyme-linked immunosorbent assay (ELISA) to determine the expression levels of IL-18 mRNA in peripheral blood mononuclear cells (PBMC) from 16 normal subjects and 18 LN patients. The results suggest that the expression of PBMCIL 18 mRNA and the level of plasma IL-18 in LN patients were significantly higher than those in normal control group [the expression of IL 18 mRNA was 1262 ± 0 189vs0 844 ± 0 15 5, P <0 01 1; IL 18 Plasma levels were (82 2 0 9 ± 5 32 77) pg / ml vs (2 39 57 ± 75 0 6) pg / ml, P <0 0 0 1]. And the increase of WHOIV-type LN was more significant than that of non-IV-type LN [the expression of IL-18 mRNA was 1 32 9 ± 0 2 1 vs 1 138 ± 0 15 2 3, P 0 05; and the plasma level of IL 18 was 1135 5 4 ± 5 15 34) pg / ml vs (5086 ± 341 36) pg / ml, P <0 0 1]. In addition, plasma IL-18 levels were correlated with renal activity index and degree of tubulointerstitial injury (r = 0 6 10 and 0 4 99 respectively, P <0.05), but also with serum creatinine (Scr) Serum endogenous creatinine clearance (Ccr) and 24 h urinary protein excretion (24 hUPQ) showed a linear correlation (r = 0 898, 0 6 2 8 and 0 5 37 respectively, P <0 05). This study suggests that elevated circulating IL-18 expression and secretion may be involved in the pathogenesis of LN and have some relationship with lupus activity