综述 Review

二甲双胍对糖尿病肾病的保护作用及其抗氧化应激机制

Published at: 2017年第37卷第4期

余丹 1 , 叶山东 1
1 安徽医科大学附属省立医院内分泌科,合肥 230001
通讯作者 山东 叶 Email: ysd196406@163.com
DOI: 10.3978/j.issn.2095-6959.2017.04.036
基金:
安徽省自然科学基金 11040606M159

摘要

高糖可以促进组织细胞活性氧(ROS)的产生,导致氧化应激,而氧化应激在糖尿病肾病(diabetic nephropathy,DN)的发生和发展中起重要作用。二甲双胍作为治疗糖尿病的一线药物,近年研究显示其除降糖作用以外,还可通过激活腺苷酸活化蛋白激酶(AMP activated protein kinase,AMPK)、磷酸化p38丝裂原活化蛋白激酶(phosphorylated p38 mitogen-activated protein kinase,p-p38MAPK),刺激醌氧化还原酶[NAD(P)H quinone oxidoreductase,NQO1]、谷胱甘肽S-转移酶a(glutathione S-transferase-a,GSTa)、过氧化氢酶(catalase,CAT)表达,阻滞晚期糖基化终末产物(advanced glycation end products,AGEs),减少GADPH氧化酶表达和改善胰岛素抵抗等机制发挥抗氧化应激作用,从而预防和延缓DN的发生和发展。


Metformin protects diabetic nephropathy and its antioxidation mechanism

Abstract

Hyperglycemia can promote the generation of reactive oxygen species and result in oxidative stress in vivo. Oxidative stress plays an important role in the occurrence and development of diabetic nephropathy (DN). Besides the hypoglycemic effect, metformin, as the first-line drug for the treatment of diabetes, can prevent and delay the occurrence and progress of DN through some antioxidation mechanisms, including activation of the AMP activated protein kinase (AMPK), phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK), stimulate the expression of NAD(P)H quinone oxidoreductase (NQO1), glutathione S-transferase-a (GSTa), and catalase (CAT), block advanced glycation end products (AGEs), reduce the expression of GADPH oxidase, improve the insulin resistance and so on.


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引用

引用本文: 丹 余, 山东 叶. 二甲双胍对糖尿病肾病的保护作用及其抗氧化应激机制[J]. 临床与病理杂志, 2017, 37(4): 862-867.
Cite this article as: YU Dan, YE Shandong . Metformin protects diabetic nephropathy and its antioxidation mechanism[J]. Journal of Clinical and Pathological Research, 2017, 37(4): 862-867.