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糖尿病视网膜病变中氧化应激相关机制及抗氧化治疗

Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Diabetic Retinopathy.

作者信息

Li Cheng, Miao Xiao, Li Fengsheng, Wang Shudong, Liu Quan, Wang Yonggang, Sun Jian

机构信息

The First Hospital of Jilin University, Changchun 130021, China.

The Second Hospital of Jilin University, Changchun 130041, China.

出版信息

Oxid Med Cell Longev. 2017;2017:9702820. doi: 10.1155/2017/9702820. Epub 2017 Feb 6.

DOI:10.1155/2017/9702820
PMID:28265339
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5317113/
Abstract

Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes and is the leading cause of blindness in young adults. Oxidative stress has been implicated as a critical cause of DR. Metabolic abnormalities induced by high-glucose levels are involved in the development of DR and appear to be influenced by oxidative stress. The imbalance between reactive oxygen species (ROS) production and the antioxidant defense system activates several oxidative stress-related mechanisms that promote the pathogenesis of DR. The damage caused by oxidative stress persists for a considerable time, even after the blood glucose concentration has returned to a normal level. Animal experiments have proved that the use of antioxidants is a beneficial therapeutic strategy for the treatment of DR, but more data are required from clinical trials. The aims of this review are to highlight the improvements to our understanding of the oxidative stress-related mechanisms underlying the development of DR and provide a summary of the main antioxidant therapy strategies used to treat the disease.

摘要

糖尿病视网膜病变(DR)是糖尿病最常见的微血管并发症之一,也是年轻成年人失明的主要原因。氧化应激被认为是DR的关键病因。高血糖水平诱导的代谢异常参与了DR的发展,并且似乎受氧化应激影响。活性氧(ROS)生成与抗氧化防御系统之间的失衡激活了多种与氧化应激相关的机制,这些机制促进了DR的发病机制。即使血糖浓度已恢复到正常水平,氧化应激造成的损伤仍会持续相当长的时间。动物实验证明,使用抗氧化剂是治疗DR的一种有益治疗策略,但临床试验还需要更多数据。本综述的目的是强调我们对DR发生发展背后氧化应激相关机制理解的进展,并总结用于治疗该疾病的主要抗氧化治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/2fb2042eb46f/OMCL2017-9702820.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/cb2047c0e726/OMCL2017-9702820.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/39c631d58226/OMCL2017-9702820.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/2b299c881b07/OMCL2017-9702820.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/caf15a0d2b76/OMCL2017-9702820.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/2fb2042eb46f/OMCL2017-9702820.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/cb2047c0e726/OMCL2017-9702820.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/39c631d58226/OMCL2017-9702820.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/2b299c881b07/OMCL2017-9702820.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/caf15a0d2b76/OMCL2017-9702820.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3beb/5317113/2fb2042eb46f/OMCL2017-9702820.005.jpg

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