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논문 기본 정보

자료유형
학술저널
저자정보
Bobae Hyun (Sahmyook University) Seulmee Shin (Sahmyook University) Aeri Lee (Sahmyook University) Sungwon Lee (Sahmyook University) Youngcheon Song (Sahmyook University) Nam-Joo Ha (Sahmyook University) Kyung-Hea Cho (Seoul Women’s University) Kyungjae Kim (Sahmyook University)
저널정보
대한면역학회 Immune Network Immune Network Vol.13 No.4
발행연도
2013.8
수록면
123 - 132 (10page)

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초록· 키워드

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Obesity is consistently increasing in prevalence and can trigger insulin resistance and type 2 diabetes. Many lines of evidence have shown that macrophages play a major role in inflammation associated with obesity. This study was conducted to determine metformin, a widely prescribed drug for type 2 diabetes, would regulate inflammation through downregulation of scavenger receptors in macrophages from obesity-induced type 2 diabetes. RAW 264.7 cells and peritoneal macrophages were stimulated with LPS to induce inflammation, and C57BL/6N mice were fed a high-fat diet to generate obesity-induced type 2 diabetes mice. Metformin reduced the production of NO, PGE2 and pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) through down-regulation of NF-κB translocation in macrophages in a dose-dependent manner. On the other hand, the protein expressions of anti-inflammatory cytokines, IL-4 and IL-10, were enhanced or maintained by metformin. Also, metformin suppressed secretion of TNF-αand reduced the protein and mRNA
expression of TNF-α in obese mice as well as in macrophages. The expression of scavenger receptors, CD36 and SR-A, were attenuated by metformin in macrophages and obese mice. These results suggest that metformin may attenuate inflammatory responses by suppressing the production of TNF-α and the expressions of scavenger receptors.

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INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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