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二甲双胍部分通过激活AMPK和抑制RAGE/NFκB途径抑制晚期糖基化终产物诱导的小鼠巨噬细胞炎症反应。

Metformin Inhibits Advanced Glycation End Products-Induced Inflammatory Response in Murine Macrophages Partly through AMPK Activation and RAGE/NFB Pathway Suppression.

作者信息

Zhou Zhong'e, Tang Yong, Jin Xian, Chen Chengjun, Lu Yi, Liu Liang, Shen Chengxing

机构信息

Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, China; Department of Cardiology, Central Hospital of Minhang District, 170 Xinsong Road, Shanghai 201199, China.

Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, China.

出版信息

J Diabetes Res. 2016;2016:4847812. doi: 10.1155/2016/4847812. Epub 2016 Sep 28.

DOI:10.1155/2016/4847812
PMID:27761470
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5059570/
Abstract

Advanced glycation end products (AGEs) are major inflammatory mediators in diabetes, affecting atherosclerosis progression via macrophages. Metformin slows diabetic atherosclerosis progression through mechanisms that remain to be fully elucidated. The present study of murine bone marrow derived macrophages showed that (1) AGEs enhanced proinflammatory cytokines (interleukin-1 (IL-1), IL-6, and tumor necrosis factor- (TNF-)) mRNA expression, RAGE expression, and NFB activation; (2) metformin pretreatment inhibited AGEs effects and AGEs-induced cluster designation 86 (CD86) (M1 marker) expression, while promoting CD206 (M2 marker) surface expression and anti-inflammatory cytokine (IL-10) mRNA expression; and (3) the AMPK inhibitor, Compound C, attenuated metformin effects. In conclusion, metformin inhibits AGEs-induced inflammatory response in murine macrophages partly through AMPK activation and RAGE/NFB pathway suppression.

摘要

晚期糖基化终末产物（AGEs）是糖尿病中的主要炎症介质，通过巨噬细胞影响动脉粥样硬化的进展。二甲双胍通过尚未完全阐明的机制减缓糖尿病动脉粥样硬化的进展。本项对小鼠骨髓来源巨噬细胞的研究表明：（1）AGEs增强促炎细胞因子（白细胞介素-1（IL-1）、IL-6和肿瘤坏死因子-（TNF-））的mRNA表达、RAGE表达和NFκB激活；（2）二甲双胍预处理可抑制AGEs的作用以及AGEs诱导的簇分化抗原86（CD86）（M1标志物）表达，同时促进CD206（M2标志物）表面表达和抗炎细胞因子（IL-10）的mRNA表达；（3）AMPK抑制剂Compound C减弱了二甲双胍的作用。总之，二甲双胍部分通过激活AMPK和抑制RAGE/NFκB途径抑制AGEs诱导的小鼠巨噬细胞炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/3bdba83b33c4/JDR2016-4847812.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/85e131966ac6/JDR2016-4847812.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/db9cd3577fbb/JDR2016-4847812.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/51bded778a0b/JDR2016-4847812.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/6a6e2429ea48/JDR2016-4847812.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/d2745cf35cd8/JDR2016-4847812.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/3bdba83b33c4/JDR2016-4847812.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/85e131966ac6/JDR2016-4847812.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/db9cd3577fbb/JDR2016-4847812.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/51bded778a0b/JDR2016-4847812.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/6a6e2429ea48/JDR2016-4847812.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/d2745cf35cd8/JDR2016-4847812.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5b/5059570/3bdba83b33c4/JDR2016-4847812.006.jpg

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