期刊
FEBS JOURNAL
卷 283, 期 12, 页码 2295-2308出版社
WILEY
DOI: 10.1111/febs.13735
关键词
advanced glycation end-product; inflammation; macrophage polarization; NF-kappa B; pioglitazone
资金
- Nature Science Foundation of China [81170193, 81470470]
Classically activated macrophages (M1) are associated with inflammation in diabetic patients. Inflammation is a known risk factor in diabetes. The present study tested the hypothesis that pioglitazone (PIO) alleviates inflammation in diabetic mice fed a high-fat diet by inhibiting advanced glycation end-product (AGE)-induced classical macrophage activation. It was found that AGE treatment promoted the transcription of pro-inflammatory molecules and M1 surface markers, whereas PIO increased the expression of anti-inflammatory genes and decreased the expression of pro-inflammatory mediators in bone marrow-derived macrophages (BMDMs) in a dose-dependent manner. Furthermore, pretreatment with PIO abrogated the effects of AGE on pro-inflammatory markers and partly inhibited AGE-induced nuclear factor-kappa B (NF-kappa B) activation. PIO treatment partly reduced the inflammatory phenotype in diabetic ApoE(-/-) mice, and significantly reduced NF-kappa B activation in plaques. Therefore, we conclude that PIO blocks classical activation of macrophages and attenuates inflammation in mouse models of diabetes.
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