scholarly journals Rutin inhibited the advanced glycation end products-stimulated inflammatory response and extra-cellular matrix degeneration via targeting TRAF-6 and BCL-2 proteins in mouse model of osteoarthritis

Aging ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 22134-22147
Author(s):  
Xiang Chen ◽  
Mingchuan Yu ◽  
Wei Xu ◽  
Linfeng Zou ◽  
Jing Ye ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mouse Model ◽  
Advanced Glycation End Products ◽  
Extra Cellular Matrix ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Cellular Matrix

Blockade of TGF-β-activated kinase 1 prevents advanced glycation end products-induced inflammatory response in macrophages

Cytokine ◽  
2016 ◽  
Vol 78 ◽  
pp. 62-68 ◽  
Author(s):  
Xingxin Xu ◽  
Xiangming Qi ◽  
Yunxia Shao ◽  
Yuanyuan Li ◽  
Xin Fu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

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

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Zhong’e Zhou ◽  
Yong Tang ◽  
Xian Jin ◽  
Chengjun Chen ◽  
Yi Lu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mrna Expression ◽  
Advanced Glycation End Products ◽  
Ampk Activation ◽  
Advanced Glycation ◽  
Murine Macrophages ◽  
Atherosclerosis Progression ◽  
Compound C ◽  
Glycation End Products ◽  
End Products

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-1β(IL-1β), IL-6, and tumor necrosis factor-α(TNF-α)) mRNA expression, RAGE expression, and NFκB 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/NFκB pathway suppression.

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