摘要
目的:糖尿病肾病及其引起的终末期肾病近年来在全球的发病情况逐年提高,该病预后差、治疗费用高,成为世界范围内严重危害人类健康的公共卫生问题。糖尿病肾病发病机制错综复杂,氧化应激被认为是重要的共同的机制之一。本文探讨氧化应激对糖尿病肾病的影响。资料来源:应用计算机检索MEDLINE,CBM,CNKI数据库及手工检索1997-01/2006-11期间的相关文献。包括临床研究(不限研究对象的年龄、性别、种族。)和基础研究,不限体内或体外研究。中文检索词包括“氧化应激”,“活性氧类”,“糖尿病肾病”和“发病机制”;英文检索词有“diabetic nephropathies”,“oxidative stress”,“reactive oxygen species”,“PKC”和“TGF-β”。资料选择:共收集到相关文献991篇,阅读全部文章的文题和大部分文章的摘要。选择文献所述内容与糖尿病肾病时氧化应激作用相关的文献。排除重复性研究和Meta分析类文章。资料提炼:共得到符合纳入条件的文献142篇,排除849篇。选择其中30篇进行分析,其中英文25篇,中文5篇,英文有1篇为手工检索的增刊。资料综合:糖尿病肾病的发病机制错综复杂,肾脏的结构和功能变化包括高滤过、肾脏和肾小球的肥大、细胞外基质的堆积、肾小球基底膜的增厚和肾小球滤过屏障功能的异常。这些变化是多因素共同作用的结果,在众多发病机制中,氧化应激被认为是共同机制之一。在正常情况下,活性氧的产生和抗活性氧水平二者处于平衡状态,当活性氧蓄积过多就会攻击机体,即氧化应激。氧化应激的产生主要是活性氧类产生过多和清除减少以及糖尿病肾病患者体内氧化应激水平增加导致的。氧化应激对糖尿病肾病的影响包括活性氧类可以增加细胞膜的通透性;使肾细胞内的谷胱甘肽过氧化物酶、超氧化物歧化酶和过氧化氢酶等抗氧化酶发生糖化或氧化,肾组织抗氧化能力降低,细胞内关键酶和转运蛋白Na-K-ATP酶失活等。结论:氧化应激作用可以增加细胞膜的通透性,使肾组织抗氧化能力降低,是糖尿病肾病的重要发病机制之一。
OBJECTIVE： The incidence of diabetic nephropathies and its end-stage renal disease is increasing year by year and is becoming a public healthy problem seriously impairing peoples＇ health in the world due to poor prognosis and expensive cost. The pathogenesy of diabetic nephropathies is very intricate, and oxidative stress is regarded as one of the significant common mechanisms. In this article, the influence of oxidative stress on diabetic nephropathies is explored.
DATA SOURCES： A computerized online databases of Medline, CBM, and CNKI, and a manual search in library were undertaken to identify the related articles dated from January 1997 to November 2006 with the English keywords of diabetic nephropathies, oxidative stress, reactive oxygen species, PKC, TGF-β and Chinese keywords of oxidative stress, reactive oxygen species, diabetic nephropathies, pathogenesy. The clinical studies regardless of age, sex, and race and basic studies were involved either in vivo or vitro.
STUDY SELECTION： Totally 991 articles were collected, and the studies that were related to the oxidative stress in diabetic nephropathies were selected, and the repeated studies and Meta analysis articles were excluded.
DATA EXTRACTION： 142 articles were included, and 849 were excluded. Among the 142 studies, 30 were selected as references including 25 in English and 5 in Chinese. Additionally, one English study was searched by hand as published in supplementary issue.
DATA SYNTHESIS： The pathogenesy of diabetic nephropathies is very complicated. The changes in renal structure and function consist of high filtration, kidney and glomeruli hypertrophia, accumulation of extracellular matrix, glomerular basement membrane thickening, and abnormal function of glomeruli filtration barrier. Those changes are caused by multiple factor. Among various nosogenesis, oxidative stress is regarded as one of the common mechanisms. Under normal condition, the production of active oxygen is balancing with anti-active oxygen; over accumulated active oxygen would attack the body, that is the oxidative stress. Oxidative stress is caused by the over production and clearance decrease of active oxygen species as well as the increase of the oxidative stress level in patients with diabetic nephropathies. The influence of oxidative stress on patients with diabetic nephropathies involves that it could increase the permeability of cell membrane, induce the saccharify or oxidation of glutathione peroxidase, superoxide dismutase, catalase in renal cells, decrease the anti-oxidation ability of renal tissue, and lead to enzyme inactivation of intraceliutar key enzyme and transport protein Na-K-ATPase.
CONCLUSION： Oxidative stress might increase the permeability of cell membrane, and reduce the anti-oxidation ability of renal tissue. It is one of the important pathogenesy for diabetic nephropathies.
出处
《中国组织工程研究与临床康复》
CAS
CSCD
北大核心
2007年第25期4988-4991,共4页
Journal of Clinical Rehabilitative Tissue Engineering Research
