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作 者:赵德安[1] 马振林[2] 王凌超 贾妮旦 刘海玉[1] ZHAO Dean;MA Zhenlin;WANG Lingchao(Department of Pediatrics,The First Affiliated Hospital of Xinxiang Medical Uuniversity,Weihui,453100)
机构地区:[1]新乡医学院第一附属医院儿内科,卫辉453100 [2]河南省周口市中心医院儿科,周口466000
出 处:《中国中西医结合肾病杂志》2019年第5期402-405,共4页Chinese Journal of Integrated Traditional and Western Nephrology
基 金:河南省卫生医学科技攻关项目(No.200703075);新乡医学院科研项目(No.2007YJA05)
摘 要:目的:微小病变型肾病综合征(MCNS)是儿童原发性肾病综合征(INS)最为常见的病理类型。对于MCNS的发病机制目前仍不是很清楚。本文观察Toll样受体-2(TLR-2)、单核巨噬细胞表面特异性标志抗原(ED-1)和白介素-1β(IL-1β)在儿童微小病变型肾病(MCNS)肾组织中的表达情况,探讨TLR-2、ED-1、IL-1β在MCNS发病过程中的作用。方法:遴选2013.01~2015.12间2岁~14岁新乡医学院第一附属医院临床表现原发性肾病综合征(INS)且病理确诊为MCNS病例20例,10例儿童肾肿瘤切除术后远离肾肿瘤边缘正常肾组织作为对照组。应用免疫组织化学染色GTVision Ⅲ二步法,对MCNS患儿肾活检肾组织切片行TLR-2、ED-1和IL-1β免疫组织化学染色。结果:正常对照组肾小球及肾小管内TLR-2、ED-1、IL-1β无或有极微量表达。与对照组比较,MCNS组TLR-2、ED-1、IL-1β在肾小球(0.47±0.17vs5.15±0.21,0.55±0.14vs22.06±0.32,0.29±0.12vs17.43±0.34;P均<0.05)和肾小管上皮(0.31±0.20vs79.45±3.65,0.84±0.39vs82.56±5.3,0.47±0.25vs63.34±4.36;P均<0.01)表达均显著增高。结论:TLR-2在肾组织高表达可能诱导肾脏固有巨噬细胞释放炎症细胞因子IL-1β的过度释放,介导MCNS的局部损伤和炎症反应,促进MCNS的进展。Objective:Minimal change nephrotic syndrome(MCNS)is an idiopathic nephrotic syndrome(INS)that is common among children. The pathogenesis of MCNS remains to be elucidated. The article will investigate the impressions of toll like receptor-2(TLR-2), Monocyte macrophage surface specific antigen (ED-1)and nterleukin-1β(IL-1β) in renal tissue of MCNS and the role of TLR-2, ED-1 and IL-1β in he pathogenesis of MCNS. Methods:20 INS children with MCDS proved by renal biopsy were obtained from Jan. 2013 to Dec. 2015 in the first affiliated hospital of Xinxing Medical University. 10 cases of children with partial nephrectomy for tumours were enrolled as control group and normal renal tissue away from kidney neoplasms confirmed by light microscopy were selected to use for clinical trials. Immunohistochemical staining(GTVision III two-step method)was used to detect the impressions of TLR-2, ED-1 and IL-1β. All cases were performed in paraffin sections of MCNS group and control group. Results:Under the light microscope, renal tubules, glomerulus and basement membrane were normal. However, effacement of the epithelial cell(podocyte)foot processes and loss of the normal charge barrier was observed under electron microscope. Compared with normal control group, impressions of TLR-2,ED-1 and IL-1β in the MCNS children was significantly higher in glomorular(0.47± 0.17 vs 5.15±0.21,0.55±0.14 vs 22.06±0.32,0.29±0.12 vs 17.43±0.34;P <0.05) and renal tubular epithelial cells (0.31± 0.20 vs 79.45±3.65,0.84±0.39 vs 82.56±5.3,0.47±0.25 vs 63.34±4.36;P <0.01). Conclusion:Increased activation of TLR-2 stimulates intrinsic acrophages to release IL-1βand mediates injury and inflammation response. So TLR-2 mediates and exacerbates possibly the progression of MCNS in children.
关 键 词:Toll样受体 细胞因子 微小病变型肾病综合征 肾活检 儿童
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