Location

Georgia

Start Date

16-5-2017 1:00 PM

Description

Anti-inflammatory, anti-oxidant, and anti-cancer effects of xanthohumol (XN), a prenylated chalcone extracted from common hop plants, are gaining attention and research has been expanding on the beneficial effects of this compound. In this study, we have investigated the anti-inflammatory effects of XN using a mouse monocytic cell line, RAW 264.7. We hypothesized that the anti-inflammatory effects of XN are due to M2 polarization of macrophages which, in turn, is mediated partly through the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. RAW 264.7 cells were treated with either 0.1% DMSO or XN at varying concentrations for 24hrs. Cell culture supernatant was collected for ELISA and whole cell lysates were collected for Western blotting experiments. Our results suggest that XN upregulated the secretion of interleukin 10 (IL10), a signature cytokine for M2 polarization, in RAW 264.7 cells after 24 hours. We further demonstrated that XN increased arginase expression, a marker for M2 polarization, and failed to increase inducible nitric oxide synthase (iNOS) expression, a marker for M1 polarization. XN decreased interferon-γ (IFNγ) induced elevation of nitrite release, indicating the inhibitory effects of XN against M1 polarization. Additionally, XN at 25µM increased the secretion of catecholamines from macrophages comparable to interleukin 4 (IL4), an inducer of the M2 phenotype. Finally, XN upregulated the expression of phospho-AMPK in RAW 264.7 cells, indicating the role of AMPK signaling pathway in XN-induced effects. These results provide evidence for the anti-inflammatory properties of XN–mediated induction of M2 polarization. The M2 macrophage mediated anti-inflammatory effects, coupled with catecholamine secretion, and previously anti-adipogenic effects, makes XN an attractive molecule to study its beneficial effects on metabolic disease, like obesity and diabetes, that are associated with underlying chronic, low-grade inflammation.

Embargo Period

6-26-2017

COinS
 
May 16th, 1:00 PM

Xanthohumol Stimulates the Secretion of Catecholamines and Induces M2 Polarization in Raw 264.7 Macrophages

Georgia

Anti-inflammatory, anti-oxidant, and anti-cancer effects of xanthohumol (XN), a prenylated chalcone extracted from common hop plants, are gaining attention and research has been expanding on the beneficial effects of this compound. In this study, we have investigated the anti-inflammatory effects of XN using a mouse monocytic cell line, RAW 264.7. We hypothesized that the anti-inflammatory effects of XN are due to M2 polarization of macrophages which, in turn, is mediated partly through the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. RAW 264.7 cells were treated with either 0.1% DMSO or XN at varying concentrations for 24hrs. Cell culture supernatant was collected for ELISA and whole cell lysates were collected for Western blotting experiments. Our results suggest that XN upregulated the secretion of interleukin 10 (IL10), a signature cytokine for M2 polarization, in RAW 264.7 cells after 24 hours. We further demonstrated that XN increased arginase expression, a marker for M2 polarization, and failed to increase inducible nitric oxide synthase (iNOS) expression, a marker for M1 polarization. XN decreased interferon-γ (IFNγ) induced elevation of nitrite release, indicating the inhibitory effects of XN against M1 polarization. Additionally, XN at 25µM increased the secretion of catecholamines from macrophages comparable to interleukin 4 (IL4), an inducer of the M2 phenotype. Finally, XN upregulated the expression of phospho-AMPK in RAW 264.7 cells, indicating the role of AMPK signaling pathway in XN-induced effects. These results provide evidence for the anti-inflammatory properties of XN–mediated induction of M2 polarization. The M2 macrophage mediated anti-inflammatory effects, coupled with catecholamine secretion, and previously anti-adipogenic effects, makes XN an attractive molecule to study its beneficial effects on metabolic disease, like obesity and diabetes, that are associated with underlying chronic, low-grade inflammation.