糖尿病肾病抗炎治疗的研究进展

糖尿病肾病（DN）是糖尿病（DM）严重的慢性并发症，由于近年来DM的发病率逐年上升，DN已成为最常见的继发性肾脏病，在大多数国家，DN已成为终末期肾病（ESRD）的最多见原因之一，但有关DN的发病机制，迄今尚未完全阐明，也缺乏有效的治疗方法。虽然糖代谢紊乱及血流动力学障碍是DN的发病基础，但并不是导致DN进展的唯一原因。近年来的研究发现，DM体内多种炎症因子、炎性介质的标志物增高，且DM的许多重要并发症如动脉粥样硬化、肾脏损害都与炎症密切相关，因而有人提出DM是一种糖脂代谢紊乱引起的炎症性疾病。研究发现，DM正常蛋白尿、微量白蛋白尿及临床蛋白尿期急性时相蛋白如C反应蛋白（CRP）、α1-酸性糖蛋白、铜蓝蛋白及唾液酸等均高于正常对照组，说明DM体内处于慢性炎症状态，同时发现，这些炎性蛋白随着微量白蛋白尿增加而增加，说明慢性炎症与肾脏损害密切相关。     

炎症在糖尿病肾病发病中的作用

糖尿病肾病的发病受多方面因素影响，越来越多的证据显示炎症在糖尿病肾病的发生发展中起重要作用。本文对炎症在糖尿病肾病发病中的作用作一综述。     

炎症在糖尿病肾病发病中的作用

糖尿病肾病的发病受多方面因素影响,越来越多的证据显示炎症在糖尿病肾病的发生发展中起重要作用。本文对炎症在糖尿病肾病发病中的作用作一综述。     

霉酚酸酯在糖尿病肾病炎症反应过程中的应用展望

糖尿病肾病是糖尿病最常见和最严重的慢性并发症之一,多种病理机制参与其发病过程,但目前确切机制尚不清楚.既往的研究主要集中在血糖和血脂代谢紊乱,血流动力学异常等方面.近年来,随着人们对糖尿病肾病发病机制的进一步认识,确立了炎症反应在糖尿病肾病进展中的作用,为抗炎治疗在糖尿病肾病中的运用提供了理论基础[1].     

TLRs与糖尿病肾病

糖尿病肾病（ Diabetic Nephropathy， DN）是糖尿病重要的微血管病变之一，现已成为终末期肾衰和糖尿病患者死亡的重要原因之一。以往我们认为其发病主要与高血糖及血流动力学改变等因素有关，而非炎症性疾病，但实验发现即使在严格控制血糖血压情况下，一部分患者仍进展为终末期肾衰，因此推测可能有其他因素参与糖尿病肾病的发生发展。近年来炎症反应参与糖尿病肾病的发病机制越来越受到人们的关注，本文主要对炎症反应重要介质－TLRs（ Toll－Like receptors）家族成员尤其是 TLR4在糖尿病肾病发病机制中的作用进行综述。     

糖尿病肾病发病炎症机制研究进展

越来越多的实验与临床研究表明炎症是糖尿病肾病(Diabetic nephropathy,DN)发生与持续进展的关键因素，本文概述了DN发病炎症实验与临床研究证据、可能的机制及干预措施，为进一步延缓或逆转DN的进展提供新的方向。     

糖尿病肾病发病炎症机制研究进展

越来越多的实验与临床研究表明炎症是糖尿病肾病(Diabeticnephropathy,DN)发生与持续进展的关键因素,本文概述了DN发病炎症实验与临床研究证据、可能的机制及干预措施,为进一步延缓或逆转DN的进展提供新的方向。     

炎症与糖尿病肾病研究的新认识

炎症能引起糖尿病肾病，并在糖尿病肾病进展的整个过程中起了重要作用。目前已有学者在动物模型中应用抗炎治疗，延缓了糖尿病肾病的进展。     

蛋白质组学及其在糖尿病肾病中的应用

蛋白质组学是一门以蛋白质组为研究对象，在蛋白质水平上对疾病机理、细胞模式、功能联系等方面进行探索的科学。其核心技术有二维凝胶电泳、质谱分析、蛋白质组信息学。其在探讨糖尿病肾病的发病机制及早期诊断中的应用前景十分广阔。     

蛋白质组学及其在糖尿病肾病中的应用

蛋白质组学是一门以蛋白质组为研究对象 ,在蛋白质水平上对疾病机理、细胞模式、功能联系等方面进行探索的科学。其核心技术有二维凝胶电泳、质谱分析、蛋白质组信息学。其在探讨糖尿病肾病的发病机制及早期诊断中的应用前景十分广阔。     

The role of inflammatory cytokines in diabetic nephropathy

Cytokines act as pleiotropic polypeptides regulating inflammatory and immune responses through actions on cells. They provide important signals in the pathophysiology of a range of diseases, including diabetes mellitus. Chronic low-grade inflammation and activation of the innate immune system are closely involved in the pathogenesis of diabetes and its microvascular complications. Inflammatory cytokines, mainly IL-1, IL-6, and IL-18, as well as TNF-alpha, are involved in the development and progression of diabetic nephropathy. In this context, cytokine genetics is of special interest to combinatorial polymorphisms among cytokine genes, their functional variations, and general susceptibility to diabetic nephropathy. Finally, the recognition of these molecules as significant pathogenic mediators in diabetic nephropathy leaves open the possibility of new potential therapeutic targets.     

联合疗法对糖尿病肾病的疗效观察

本研究采用血管紧张素转换酶抑制剂(ACEI)、他汀类药物、内皮素受体拈抗剂(ETRA)联合治疗糖尿病肾病(DN),观察其疗效. 一、对象与方法 1.病例:2005年12月至2007年12月本院肾内科与内分泌科住院及门诊DN患者60例为对象,均符合WHO 2型糖尿病诊断及Mogensen分期标准.     

氯沙坦对糖尿病肾病大鼠炎性反应的抑制作用

糖尿病肾病（DN）是糖尿病（DM）全身微血管病变的表现之一，其发生机制十分复杂。近年来炎性反应学说备受关注，且随着对血管紧张素受体拈抗剂（ARB）类药物研究的日益增多，发现其尚可通过抑制慢性亚临床炎性反应而发挥肾脏保护作用，但机制尚未完全明了。奉研究观察氯沙坦对DM大鼠血CRP、TNF—α水平以及Toll样受体4（TLR4）、NF—κB在肾组织中表达的影响，对其抑制炎性反应的作用机制进行初步的探讨。     

Effect of insulin therapy on established diabetic nephropathy in rats

The effectiveness of insulin therapy on early diabetic nephropathy has not been established. In this study we examined the influence of continuous subcutaneous insulin on the progression of established nephropathy in streptozocin-induced diabetic rats. Normal controls and diabetic rats were studied for 11 mo. During the first 6 mo, all the diabetic rats received 2 U protamine zinc insulin s.c. twice weekly. During the last 5 mo of study, diabetic rats either continued on the occasional subcutaneous insulin regimen or received regular insulin by continuous subcutaneous infusion. Six months after the initiation of the study, the diabetic rats were severely hyperglycemic, and their relative mesangial areas had increased. Continued poor glycemic control in the rats receiving occasional insulin was associated with relative increased mesangial area (25.2 +/- 1.0% of glomerular area) and significant proteinuria (148 +/- 17 mg/24 h) compared with normal controls. In contrast, the use of continuous subcutaneous insulin therapy with improved glycemic control arrested mesangial changes (19.5 +/- 1.4% of glomerular area) and prevented the excessive proteinuria (71 +/- 13 mg/24 h). Indeed, these parameters did not differ from age-matched controls. We conclude that in the rat, continuous subcutaneous insulin therapy instituted after the development of early glomerular pathology is effective in arresting the disease process.     

前列地尔联合贝那普利治疗早期糖尿病肾病临床观察

目的观察前列地尔联合贝那普利治疗早期糖尿病肾病（DN）的疗效。方法将DN患者随机分为2组,在常规治疗的同时,A组服用贝那普利,B组前列地尔联合贝那普利治疗,时间均为2周,比较2组治疗前后尿自蛋白排泄率（UAER）的变化。结果两组治疗前后UAER均有显著下降（A组P〈0．05,B组P〈0．01）,B组与A组比较差异有统计学意义（P〈0．05）。结论前列地尔联合贝那普利列地尔注射液是治疗糖尿病肾病的有效方法。     

Relationship between E - cadherin and diabetic nephropathy

Objective To identify novel biomarker for diabetic nephropathy (DN) by urinary proteomic methods, and to detect the expression of E-cadherin in urine and renal tissue of patients with DN. Methods Urine samples were collected from 12 cases of type 1 diabetic nephropathy patients (T1DN), 12 cases of type 2 diabetic nephropathy patients (T2DN), 12 cases of nephritic syndrome patients (NS), and 12 cases of healthy Controls. Comparative proteomic approach of two-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS) were employed to identify DN-related biomarker in urine samples. The differential expression of the identified biomarker in urine samples and renal biopsy specimens were detected by Western blotting and immunohistochemistry method. Results E-cadherin was identified by 2DE/MS, which was significantly up-regulated in T1DN and T2DN groups (all P＜ 0.01). Western blotting confirmed the expression of E-cadherin was significantly higher in T1DN and T2DN groups than in NS and Control groups (all P＜0.01). Immunohistochemical stain showed E-cadherin was mainly expressed in the membrane and cytoplasm of renal tubular epithelial cell, and its expression was markedly decreased in DN kidneys compared with healthy Controls (P＜0.05). Conclusions E-cadherin is identified as a novel DN-related biomarker, which is specifically increased in urine of DN patients.