Chrysophanol demonstrates anti-inflammatory properties in LPS-primed RAW 264.7 macrophages through activating PPAR-γ

Chrysophanol demonstrates anti-inflammatory properties in LPS-primed RAW 264.7 macrophages... Sepsis is a life-threatening disease. Inflammation is a major concomitant symptom of sepsis Chrysophanol, an anthraquinone derivative isolated from the rhizomes of rheumpalmatum, has been reported to have a protective effect against lipopolysaccharide(LPS)-induced inflammation. However, the underlying molecular mechanisms are not well understood. The aim of this study was to explore the effect and mechanism of chrysophanol on lipopolysaccharide (LPS)-induced anti-inflammatory effect of RAW264.7 cells and its involved potential mechanism. The mRNA and protein expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-κB) and PPAR-γ were measured by qRT-PCR and western blotting, the production of TNF-α, IL-1β was evaluated by ELISA. Then, the phosphorylation of NF-κB p65 was also detected by western blotting. And NF-κB p65 promoter activity was analyzed by the Dual-Luciferase reporter assay system as well. Meanwhile, PPAR-γ inhibitor GW9662 was performed to knockdown PPAR-γ expression in cells. Our data revealed that LPS induced the up-regulation of TNF-α, IL-1β, iNOS and NF-κB p65, the down-regulation of PPAR-γ were substantially suppressed by chrysophanol in RAW264.7 cells. Furthermore, our data also figured out that these effects of chrysophanol were largely abrogated by PPAR-γ inhibitor GW9662. Taken together, our results indicated that LPS-induced inflammation was potently compromised by chrysophanol very likely through the PPAR-γ-dependent inactivation of NF-κB in RAW264.7 cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Immunopharmacology Elsevier

Chrysophanol demonstrates anti-inflammatory properties in LPS-primed RAW 264.7 macrophages through activating PPAR-γ

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Publisher
Elsevier
Copyright
Copyright © 2018 Elsevier Ltd
ISSN
1567-5769
eISSN
1878-1705
D.O.I.
10.1016/j.intimp.2018.01.023
Publisher site
See Article on Publisher Site

Abstract

Sepsis is a life-threatening disease. Inflammation is a major concomitant symptom of sepsis Chrysophanol, an anthraquinone derivative isolated from the rhizomes of rheumpalmatum, has been reported to have a protective effect against lipopolysaccharide(LPS)-induced inflammation. However, the underlying molecular mechanisms are not well understood. The aim of this study was to explore the effect and mechanism of chrysophanol on lipopolysaccharide (LPS)-induced anti-inflammatory effect of RAW264.7 cells and its involved potential mechanism. The mRNA and protein expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-κB) and PPAR-γ were measured by qRT-PCR and western blotting, the production of TNF-α, IL-1β was evaluated by ELISA. Then, the phosphorylation of NF-κB p65 was also detected by western blotting. And NF-κB p65 promoter activity was analyzed by the Dual-Luciferase reporter assay system as well. Meanwhile, PPAR-γ inhibitor GW9662 was performed to knockdown PPAR-γ expression in cells. Our data revealed that LPS induced the up-regulation of TNF-α, IL-1β, iNOS and NF-κB p65, the down-regulation of PPAR-γ were substantially suppressed by chrysophanol in RAW264.7 cells. Furthermore, our data also figured out that these effects of chrysophanol were largely abrogated by PPAR-γ inhibitor GW9662. Taken together, our results indicated that LPS-induced inflammation was potently compromised by chrysophanol very likely through the PPAR-γ-dependent inactivation of NF-κB in RAW264.7 cells.

Journal

International ImmunopharmacologyElsevier

Published: Mar 1, 2018

References

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