Journal
EBIOMEDICINE
Volume 9, Issue -, Pages 61-76Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ebiom.2016.06.017
Keywords
Obesity-related inflammation; Macrophage polarization; Apigenin; PPAR gamma; NF-kappa B
Funding
- National Natural Science Foundation of China [81273527, 81421091, 81503082, 81473220]
- Natural Science Foundation of Jiangsu Province of China [BK20150575]
- Postdoctoral Science Foundation of China [2015M570437]
Ask authors/readers for more resources
PPAR gamma has emerged as a master regulator of macrophage polarization and is the molecular target of the thiazolidinedione drugs. Here we show that apigenin binds and activates PPAR gamma by acting as a modulator. Activation of PPAR gamma by apigenin blocks p65 translocation into nuclei through inhibition of p65/PPAR gamma complex translocation into nuclei, thereby decreasing NF-kappa B activation and favoringM2 macrophage polarization. In HFD and ob/ob mice, apigenin significantly reverses M1 macrophage into M2 and reduces the infiltration of inflammatory cells in liver and adipose tissues, as well as decreases the levels of pro-inflammatory cytokines, thereby alleviating inflammation. Strikingly, apigenin reduces liver and muscular steatosis, decreases the levels of ALT, AST, TC and TG, improving glucose resistance obviously. Unlike rosiglitazone, apigenin does not cause significant weight gain, osteoporosis et al. Our findings identify apigenin as a modulator of PPAR gamma and a potential lead compound for treatment of metabolic disorders. (C) 2016 The Authors. Published by Elsevier B.V.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available