首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到18条相似文献,搜索用时 93 毫秒
1.
背景:梗阻性肾纤维化的治疗思路主要集中于解除肾结石、肾盂输尿管狭窄等危险因素以及针对上皮-间质转化、肾纤维化发生相关因子及改善肾间质微循环等肾纤维化发生机制进行,目前治疗效果并不理想。以干细胞为基础的再生医学研究有可能为梗阻性肾纤维化的治疗带来新的希望。目的:综合分析不同来源干细胞治疗梗阻性肾纤维化的机制及研究进展。方法:检索Pub Med、Ovid medline全文数据库、CNKI、维普数据库、万方数据库等并收集关于干细胞治疗梗阻性肾纤维化的文章,中文以"干细胞、梗阻性肾病、肾纤维化"为检索词,英文以"stem cells、obstructive nephropathy、renal fibrosis"为检索词进行检索,最终选择51篇文章进行总结。结果与结论:干细胞治疗梗阻性肾病尚处于实验阶段,大量研究表明干细胞移植对梗阻性肾病肾间质纤维化的治疗具有积极的作用,干细胞可移植定位于肾间质,向肾小管上皮细胞分化,促进肾纤维化的恢复,干细胞还能分泌、上调或下调一些细胞因子抗纤维化,在及时、早期解除梗阻的前提下,干细胞移植有可能为梗阻性肾纤维化恢复提供一种新型的治疗方案。  相似文献   

2.
肾脏纤维化的研究进展   总被引:10,自引:0,他引:10  
肾脏纤维化是所有慢性肾脏疾病发展的最终结果.促纤维化因子的释放在肾脏纤维化的形成中起重要作用.目前对肾脏纤维化治疗的研究主要集中在抑制肾纤维细胞的活性以及抑制胶原的形成,而中草药的研究、基因治疗的出现使肾脏纤维化的治疗手段呈现新的突破.  相似文献   

3.
糖尿病肾病是糖尿病三大微血管并发症之一,流行病学调查结果显示,2型糖尿病肾病的发生率为20%一60%,是终末期肾衰的主要原因之一,主要病理特征为肾纤维化,在临床上早期发现肾纤维化并早期防止纤维化的发展,是预防慢性肾功能衰竭的最好方法。目前,临床上肾纤维化诊断有赖于肾脏病理学诊断,而肾活检是一种有创性检查。近年的研究表明,肝纤维化指标四项[透明质酸(HA)、层黏连蛋白(LN)、Ⅲ型前胶原氨端肽(PIIIP)、Ⅳ型胶原(CIV)]在肾组织纤维化的发生发展中都有异常表达。为了解糖尿病患者血清中肝纤维化指标的变化,了解糖尿病患者肾纤维化的情况,本文检测了2型糖尿病(DM2)患者血清HA、LN、PⅢP和CIV水平,现报道如下。  相似文献   

4.
目的: 探讨化瘀导滞汤对庆大霉素所致的肾间质纤维化的影响及作用机制。方法: 32只健康雄性Wistar大鼠随机分为3组:正常组(6只)、肾纤维化模型组(13只)、化瘀导滞汤治疗组(13只)。肾纤维化模型组和化瘀导滞汤治疗组给予庆大霉素造成肾纤维化,造模同时,治疗组给予化瘀导滞汤煎剂灌胃干预,直至取材。于造模后30 d取材,光镜下观察肾组织形态学改变,计算肾系数、检测血肌酐、血尿素氮、24 h尿蛋白总量,检测各组大鼠肾组织α-平滑肌肌动蛋白(α-SMA)、Smad通路蛋白2(Smad2)、Smad通路蛋白7(Smad7)的表达水平。结果: 肾纤维化模型组大鼠与正常组比较,光镜下可见肾小管上皮细胞以坏死为主,部分变性,肾小管萎缩和扩张,间质中有成纤维细胞增生和炎症细胞浸润,间质明显增宽。模型组肾系数、血肌酐、血尿素氮、24 h尿蛋白总量明显高于正常组(P<0.01),α-SMA、Smad2蛋白表达明显高于正常组(P<0.01),Smad7蛋白表达明显低于正常组(P<0.01);化瘀导滞汤治疗组与肾纤维化模型组比较,光镜下肾小管结构有明显改善,治疗组肾系数、血肌酐、血尿素氮、24 h尿蛋白总量与模型组比较有显著下降(P<0.01),治疗组α-SMA、Smad2蛋白表达明显低于模型组(P<0.01),Smad7蛋白表达无明显变化(P>0.05)。结论: 化瘀导滞汤有良好的防治庆大霉素诱导的肾纤维化作用。  相似文献   

5.
肾小管上皮细胞在肾间质纤维化中的作用   总被引:5,自引:0,他引:5  
肾小管是连接肾小球与肾间质的枢纽 ,肾小管上皮细胞可通过产生趋化因子、致纤维化细胞因子、表型转化为成纤维 /肌成纤维细胞以及细胞凋亡等方式 ,主动参与肾间质纤维化的发生与发展。干预肾小管上皮细胞的表型转化及凋亡 ,可能会为抗纤维化治疗提供新的思路和手段  相似文献   

6.
肾间质纤维化是所有肾病进行性发展的最终通路,是导致终末期肾病的主要病理基础。目前研究发现,肾小管上皮转分化在肾间质纤维化的发生、发展过程中发挥重要作用。肾小管上皮在转分化过程中逐步失去其原有特征而获得肌成纤维细胞的特征,如表达α-平滑肌肌动蛋白(α-SMA),并合成细胞外基质,转化生长因子-β1(TGF-β1)被认为参与了这一过程并在其中起着十分关键的作用[1]。探索有效抑制和逆转转分化的发生,从而抑制肾间质纤维化的进展具有重要意义。本实验采用大鼠单侧输尿管结扎术(UUO)建立肾间质纤维化动物模型,用银杏叶进行治疗,选用公…  相似文献   

7.
MicroRNA-29在肾纤维化进程中的研究进展   总被引:1,自引:1,他引:0  
刘袆  孙雪娇  李城  王曦廷  李彧 《解剖学报》2017,48(5):622-627
肾纤维化是慢性肾脏疾病(CKD)发展到终末期肾衰竭的共同病理,主要表现为细胞外基质(ECM)的过度沉积。MicroRNAs(miRNAs)是一类微小非编码RNAs,通过抑制目的基因mRNAs转录后的表达而调控肾脏的生理功能及稳态。miR-29s通过调节ECM的合成与沉积以及上皮-间质转化(EMT)发挥抗纤维化作用,另外,miR-29s与多种炎症和促纤维化通路相互作用,其作为治疗肾纤维化的试剂或者靶点研究有着重要意义和广泛前景。本文中我们综述了最近有关miR-29s抗肾纤维化作用的研究成果。  相似文献   

8.
醛固酮与器官纤维化   总被引:4,自引:0,他引:4  
醛固酮 (ALD)是体内重要的盐皮质激素 ,不仅产生于肾上腺皮质球状带细胞 ,也可产生于血管、肝、肺、肾、脑等组织。研究表明 ,ALD与心肌纤维化及肺纤维化有密切关系 ,抗ALD治疗可减轻其纤维化程度。ALD可能与肾纤维化亦有关。提示ALD可能参与了体内多种器官纤维化的形成过程。  相似文献   

9.
目的:研究慢性肾衰残余肾组织血小板源生长因子-α(PDGF-α)的表达状况及其机理和意义。方法:采用斑点杂交和形态计量等方法,对假手术对照大鼠、5/6肾切除大鼠、以及5/6肾切除术后给予维生素E治疗的大鼠肾组织PDGF-αmRNA含量及其相关指标进行定量分析。结果:①5/6肾切除大鼠残存肾组织PDGF-αmRNA含量显著增高;②5/6肾切除大鼠周围血单个核细胞内游离钙浓度显著增高,细胞内游离钙浓度与PDGF-αmRNA含量成正相关;③5/6肾切除大鼠残肾组织有显著的固有细胞增殖、肾小球硬化和肾间质纤维化,肾组织羟脯氨酸含量显著增高,PDGF-αmRNA含量与硬化肾小球比率、病变肾小管和肾间质体密度、肾组织羟脯氨酸含量成正相关;④给予维生素E治疗的大鼠,随着细胞内游离钙浓度和PDGF-αmRNA含量降低,残肾硬化肾小球比率、病变肾小管和肾间质体密度、肾组织羟脯氨酸含量显著下降。结论:PDGF-α高表达可能是残存肾组织进行性纤维化的重要原因之一;维生素E治疗能降低PDGF-α表达,抑制残肾纤维化,减缓残肾毁损速度  相似文献   

10.
肾纤维化是在慢性肾脏病(CKD)进展过程中多种细胞外基质广泛沉积的结果,是CKD发展的终末阶段,患者常常需要透析或者进行肾脏移植来维持生命.肾纤维化发生的细胞及分子生物学机制目前尚不十分明确,可能与细胞内一系列细胞增殖相关的信号通路的活化、microRNA的作用、细胞的凋亡和继发性坏死、肾脏中的肌成纤维细胞的异常分化与重构有关.因而研究肾纤维化发病机制的研究进展,特别是调控细胞增殖及纤维化发生分子生物学机制及肾肌成纤维细胞的重构和异常分化对肾纤维化的影响很有意义.  相似文献   

11.
The progression of various chronic kidney disease to a certain stage leads to renal fibrosis. Renal fibrosis can be stimulated by a variety of factors, including kidney trauma, infection, blood circulation blockage or immune response, etc. After renal tissue damage caused by these factors, a large number of collagen fibers deposited in the stroma to form fibrous scars, which resulted in changes of renal structure and function and further led to renal fibrosis. So far, the mechanism of renal fibrosis remains not fully understood. The establishment of an ideal animal model is of great significance for the study of the mechanism of renal fibrosis. Numerous literatures reported the establishment of animal models of renal fibrosis through surgery. Therefore, this article focused on the methods of establishment of animal model of renal fibrosis by sur gery and the pathogenesis of renal fibrosis in recent years.  相似文献   

12.
Renal fibrosis is the culmination of processes driven by signaling pathways involving transforming growth factor-β family of cytokines, connective-tissue growth factor, nuclear factor κB, Wnt/β-catenin, Notch, and other growth factors. Many studies in experimental animal models have directly targeted these pathways and demonstrated efficacy in mitigating renal fibrosis. However, only a small fraction of these approaches have been attempted in human and even fewer have been successfully translated to clinical use for patient with kidney diseases. Drugs with proven efficacy for treatment of kidney diseases and tissue fibrosis exert some of their effects by interfering with components of these pathways. This review considers key molecular mediators of renal fibrosis and their potential as targets for treatment of renal fibrosis.  相似文献   

13.
Disturbed intrauterine development increases the risk of renal disease. Various studies have reported that Notch signalling plays a significant role in kidney development and kidney diseases. A disintegrin and metalloproteinase domain 10 (ADAM10), an upstream protease of the Notch pathway, is also reportedly involved in renal fibrosis. However, how ADAM10 interacts with the Notch pathway and causes renal fibrosis is not fully understood. In this study, using a prenatal chlorpyrifos (CPF) exposure mouse model, we investigated the role of the ADAM10/Notch axis in kidney development and fibrosis. We found that prenatal CPF-exposure mice presented overexpression of Adam10, Notch1 and Notch2, and led to premature depletion of Six2+ nephron progenitors and ectopic formation of proximal tubules (PTs) in the embryonic kidney. These abnormal phenotypic changes persisted in mature kidneys due to the continuous activation of ADAM10/Notch and showed aggravated renal fibrosis in adults. Finally, both ADAM10 and NOTCH2 expression were positively correlated with the degree of renal interstitial fibrosis in IgA nephropathy patients, and increased ADAM10 expression was negatively correlated with decreased kidney function evaluated by serum creatinine, cystatin C, and estimated glomerular filtration rate. Regression analysis also indicated that ADAM10 expression was an independent risk factor for fibrosis in IgAN. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland.  相似文献   

14.
AKI (acute kidney injury) with maladaptive repair plays exacerbated role in renal fibrosis characterized by tubulointerstitial fibrosis. Previously, we reported that IKKα contributed to kidney regeneration and inhibited inflammation. Here, we first identified the role and mechanism of IKKα on TGF-β1-induced fibrosis in human tubular epithelial cells and fibrotic kidneys. IKKα was up-regulated in kidney tubular epithelium in unilateral ureteral obstruction (UUO) and unilateral ischemic reperfusion injury (UIRI) mice. Immunohistochemical staining showed that IKKα was positively correlated with the extent of kidney fibrosis in tissue biopsies from chronic kidney disease (CKD) patients. Compared with wild-type controls, Ksp-IKKα−/− mice exhibited inactivated Wnt/β-catenin pathway, decreased serum creatinine and interstitial fibrosis in the kidney after IRI. In TGF-β1-stimulated human tubular epithelial cells, IKKα overexpression enhanced β-catenin nuclear translocation. Blocking IKKα by siRNA specifically suppressed β-catenin activation and downstream profibrotic genes such as fibronectin and α-smooth muscle actin (α-SMA). Taken together, our study demonstrated that IKKα aggravated renal fibrogenesis by activating Wnt/β-catenin signalling pathway, providing a new target for the treatment of kidney fibrosis.  相似文献   

15.
Two autopsy cases of renal hypertension with hydronephrotic pyelonephritis due to fibrous retroperitonitis are reported.
The first case suffered from continuous hypertension, inspite of nephrectomy of the left kidney which was conspicuously atrophic and showed marked hydroureter due to proliferative endoarteritis of the left renal artery and retroperitoneal fibrosis. On autopsy, there was compensatory hypertrophy of the right kidney with partial cicatrical contraction due to obstructive endoarteritis of the lower branch of the right renal artery. The retroperitoneal fibrosis extended from the pericystic area to the upper abdomen.
The second case had two remarkable changes, one of which was atrophy of the right kidney due to proliferative endoarteritis of the stem of the right renal artery and another was bilateral hydronephrotic pyelonephritis owing to retroperitoneal fibrosis.
Moreover, systemic proliferative vasculitis were found in both cases.
The relationship of these lesions was discussed.  相似文献   

16.
The demands for kidney transplantations are increasing, and so is the number of live kidney donors (LKDs). Recent studies show that LKDs have an increased risk of developing end-stage renal disease compared with healthy non-donors. However, the knowledge about factors predicting renal disease in kidney donors is sparse. Some evidence points to increased glomerular sclerosis and kidney fibrosis, as well as a low number of glomeruli as associated with a worse renal outcome. This methodological study investigated that which estimates are obtainable with a standard kidney biopsy taken from the donated kidney during the transplantation, and a standard contrast-enhanced computed tomography (CT) in kidney donors. CT-scans were used to obtain total volume of the kidney and kidney cortex using the Cavalieri estimator and 2D-nucleator. Glomerular number density in the biopsies was estimated by a model-based method, and was multiplied by total cortex volume in order to estimate the total number of glomeruli in the kidney. Glomerular volume was estimated by the 2D-nucleator and a model-based stereological technique. Kidney fibrosis (point-counting), glomerular sclerosis (evaluation of glomerular profiles), and arteriole dimensions (2D-nucleator) were also estimated in the biopsy sections from the donated kidney. Various studies have attempted to identify predictors of renal outcome in LKDs. There is no consensus yet, and further studies are needed to elucidate if and how the estimates described in this study are associated with renal outcome in LKDs.  相似文献   

17.
18.
The clinical application of gentamicin has been limited by its nephrotoxicity, which is characterized by kidney injury, interstitial fibrosis and progressive renal impairment. In this paper, we examine effects of plasmid pUDK-HGF which encodes the human hepatocyte growth factor (HGF) gene on gentamicin-induced renal injury in rats. The kidney injury was intentionally induced by injecting gentamicin intraperitoneally. On the third day after last gentamicin treatment, pUDK-HGF was injected into the left kidney tissue only once via a sterile back incision. At day 30 after gentamicin treatment, RI, Scr, BUN, 24h-UTP and apoptotic cell death were determined. Tubulointerstitial injury and the renal interstitial vessel regeneration were evaluated by histological scoring. pUDK-HGF treatment significantly improved the renal function with decreasing RI, Scr and BUN. 24h-UTP also presented ameliorating trend compared to the control group with kidney injury. pUDK-HGF treatment significantly decreased the score of tubulointerstitial injury and enhanced angiogenesis, also prevented kidney cells from apoptosis. The tubulointerstitial injury was significantly reduced in the pUDK-HGF injected left kidney and right kidney also showed some improvements. Our results showed that pUDK-HGF may become a novel therapeutic agent for kidney injury and renal fibrosis.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号