Metformin Modulates Inflammatory Response through AMPK-NF-κB Signaling and Restores Atherogenic Effects
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1
Sahmyook University, Republic of Korea
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2
Seoul Women's University, Republic of Korea
Metformin is one of the most widely prescribed drugs for the treatment of type II diabetes. Metformin has been reported to mediate inflammatory responses and attenuate development of atherosclerosis besides its antihyperglycemic effect. But the pharmacological and biochemical mechanisms of metformin in immune responses and atherogenesis have not been clearly elucidated. Here we demonstrate that metformin down-regulates pro-inflammatory cytokines and foam cell formation in macrophages. Metformin reduced the production of NO through the suppressed gene and protein expression of iNOS in LPS-stimulated RAW 264.7 cells and peritoneal macrophages. Metformin antagonized the production of proinflammatory cytokines such as TNF-α, IL-1β, and IL-6, leading to suppressed the phosphorylation of IκBα and the translocation of NF-κB p65 subunit into nuclear. Furthermore, scavenger receptors (SR-A, Lox-1) mRNA levels were down-regulated by metformin. These results show that metformin attenuates inflammatory mediators via AMPK-NF-κB signaling, suggesting that metformin would be a potential immunemodulatory agent for treating vascular inflammatory diseases.
Keywords:
Metformin,
Inflammation,
scavenger receptors,
NF-κB,
AMPK
Conference:
15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013.
Presentation Type:
Abstract
Topic:
Immune-mediated disease pathogenesis
Citation:
Hyun
B,
Shin
S,
Lee
A,
Lee
S,
Song
Y,
Cho
K and
Kim
K
(2013). Metformin Modulates Inflammatory Response through AMPK-NF-κB Signaling and Restores Atherogenic Effects.
Front. Immunol.
Conference Abstract:
15th International Congress of Immunology (ICI).
doi: 10.3389/conf.fimmu.2013.02.00183
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Received:
11 Mar 2013;
Published Online:
22 Aug 2013.
*
Correspondence:
Prof. Kyungjae Kim, Sahmyook University, Seoul, Republic of Korea, kimkj@syu.ac.kr