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目的研究泛素连接酶Parkin在糖尿病肾病(diabetic nephropathy,DN)患者肾组织中的表达规律及与肾小管间质损伤的关系。方法纳入2015-2016年我院收治的40例经肾活检确诊为2型DN患者,并取10例肾肿瘤切除后远端正常肾组织为对照组。采用免疫组化检测不同DN间质损伤评分肾组织的Parkin表达水平,并与临床指标、肾组织病理损伤进行相关性分析。免疫荧光共染检测肾小管Parkin的表达分别与肾间质损伤因子IL-6、TGF-β的表达及间质纤维化标志Col-Ⅳ的表达的关系。结果 Parkin主要在肾小管上皮细胞细胞质中表达,并随着DN肾小管间质损伤评分的加重而逐渐减少。Parkin表达与肾脏结构损伤(肾小球硬化、肾小管萎缩与间质纤维化、肾间质炎症)评分呈显著负相关(P<0.01),与肾脏功能损伤指标[尿蛋白定量、尿N-乙酰-β-氨基葡萄糖苷酶(NAG)、尿素氮、血清胱抑素C、血肌酐]呈负相关关系(P<0.01),与肾小球滤过率呈正相关关系(P<0.05)。肾组织Parkin阳性肾小管细胞并不表达促炎因子IL-6、促纤维化因子TGF-β及Col-Ⅳ。结论 Parkin表达降低与DN肾间质损伤密切相关。
Objective To investigate the expression of Parkin in renal tissue of patients with diabetic nephropathy (DN) and its relationship with tubulointerstitial injury. Methods Forty patients with type 2 DN confirmed by renal biopsy were enrolled in our hospital from 2015 to 2016. Ten normal renal tissues were removed after renal tumor resection as the control group. Immunohistochemistry was used to detect the expression of Parkin in different DN interstitial injury scores, and the correlation was analyzed with clinical indicators and pathological changes of renal tissue. Immunofluorescence staining was used to detect the expression of tubular Parkin in renal interstitium and the expression of interstitial fibrosis markers Col-Ⅳ and IL-6 and TGF-β. Results Parkin was mainly expressed in the cytoplasm of renal tubular epithelial cells and gradually decreased with the increase of DN tubulointerstitial injury score. There was a significant negative correlation between the expression of Parkin and the score of renal structural damage (glomerulosclerosis, tubular atrophy and interstitial fibrosis, interstitial fibrosis) (P <0.01) Β-glucosaminidase (NAG), blood urea nitrogen, serum cystatin C and serum creatinine (P <0.01), and had a positive correlation with glomerular filtration rate (P <0.05). Renal tubular Parkin-positive tubular cells do not express proinflammatory cytokines IL-6, pro-fibrosis factor TGF-β and Col-Ⅳ. Conclusions The decrease of Parkin expression is closely related to the damage of renal interstitium in.