CAJ | 학술논문

目的：探讨高迁移率族蛋白B1( HMGB1)及晚期糖基化终产物受体(RAGE)在狼疮性肾炎(LN)中的作用。方法 ELISA法检测系统性红斑狼疮( SLE )患者及正常对照者血清、尿液中 HMGB1的表达水平,免疫组化法检测 SLE患者及正常对照者肾组织中HMGB1及RAGE的表达水平。结果 SLE患者血清及尿液的HMGB1水平与正常对照者比较均升高(P<0．01),活动期SLE患者较稳定期SLE患者明显升高(P<0．05)。狼疮肾损害者血清HMGB1水平明显高于狼疮非肾损害者(P<0．05)且与SLE疾病活动指数(SLE-DAI)评分、24 h尿蛋白定量、白细胞计数呈正相关性( P<0．05),尿液中HMGB1水平与 SLEDAI评分呈正相关性(P<0．05)。正常对照者肾组织肾小管上皮细胞可中等强度表达HMGB1和RAGE,肾小球未见表达；而在SLE患者可见肾小管中表达有所增强,肾小球中也明显表达,其肾内的HMGB1和RAGE的表达水平较正常对照者明显增加( P<0．05)；Ⅳ型、Ⅳ+Ⅴ型SLE患者肾内HMGB1的表达量均明显高于Ⅱ型(P<0．05),Ⅳ型SLE患者肾内RAGE的表达量高于Ⅱ型(P<0．05)。结论 HMGB1和RAGE可能参与了LN的发病过程,与疾病的病理变化有关。
목적：탐토고천이솔족단백B1( HMGB1)급만기당기화종산물수체(RAGE)재랑창성신염(LN)중적작용。방법 ELISA법검측계통성홍반랑창( SLE )환자급정상대조자혈청、뇨액중 HMGB1적표체수평,면역조화법검측 SLE환자급정상대조자신조직중HMGB1급RAGE적표체수평。결과 SLE환자혈청급뇨액적HMGB1수평여정상대조자비교균승고(P<0．01),활동기SLE환자교은정기SLE환자명현승고(P<0．05)。랑창신손해자혈청HMGB1수평명현고우랑창비신손해자(P<0．05)차여SLE질병활동지수(SLE-DAI)평분、24 h뇨단백정량、백세포계수정정상관성( P<0．05),뇨액중HMGB1수평여 SLEDAI평분정정상관성(P<0．05)。정상대조자신조직신소관상피세포가중등강도표체HMGB1화RAGE,신소구미견표체；이재SLE환자가견신소관중표체유소증강,신소구중야명현표체,기신내적HMGB1화RAGE적표체수평교정상대조자명현증가( P<0．05)；Ⅳ형、Ⅳ+Ⅴ형SLE환자신내HMGB1적표체량균명현고우Ⅱ형(P<0．05),Ⅳ형SLE환자신내RAGE적표체량고우Ⅱ형(P<0．05)。결론 HMGB1화RAGE가능삼여료LN적발병과정,여질병적병리변화유관。
Objective To explore the role of high mobility group box protein 1 ( HMGB1 ) and receptor for ad-vanced glycation endproducts( RAGE) in lupus nephritis( LN) . Methods The serum and urine levels of HMGB1 were detected by ELISA in SLE patients and normal controls, and intrarenal expressions of HMGB1 and RAGE were detected by immunohistochemistry in renal tissues of SLE patients and normal-appearing renal tissues. Results <br> The serum and urine levels of HMGB1 were significantly higher in SLE patients compared to healthy controls( P<0. 01 ) , in patients with active disease compared to those with inactive disease ( P <0. 05 ) , serum levels of HMGB1 were found to be significantly higher in patients with renal involvement compared to those without renal in-volvement(P<0. 05). In addition, the levels of serum HMGB1 showed positive correlation with SLEDAI,urine pro-tein(24 h) and lencocyte count (P <0. 05). The expression of urine HMGB1 showed positive correlation with SLEDAI ( P<0. 05 ) . Intermediate-intensity staining of HMGB1 and RAGE was detected in renal tubules in normal-appearing renal tissues, however, both renal tubules and glomerular cells had the strong expression of HMGB1 and RAGE in SLE patients. The intrarenal production of HMGB1 and RAGE in SLE patients was obviously higher than that in normal-appearing renal tissues(P<0. 05), and the expression levels of HMGB1 in SLE IV and IV+V were higher than those in SLE II ( P<0. 05 ) . The expression levels of RAGE in SLE IV were higher than those in SLE II(P<0. 05). Conclusion HMGB1 and RAGE may play key roles in the pathogenesis of LN and may associate with the pathology category of LN.