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Wogonin prevents lipopolysaccharide‐induced acute lung injury and inflammation in mice via peroxisome proliferator‐activated receptor gamma‐mediated attenuation of the nuclear factor‐kappaB pathway

Wogonin prevents lipopolysaccharide‐induced acute lung injury and inflammation in mice via... Acute lung injury (ALI) from a variety of clinical disorders, characterized by diffuse inflammation, is a cause of acute respiratory failure that develops in patients of all ages. Previous studies reported that wogonin, a flavonoid‐like chemical compound which was found in Scutellaria baicalensis, has anti‐inflammatory effects in several inflammation models, but not in ALI. Here, the in vivo protective effect of wogonin in the amelioration of lipopolysaccharide (LPS) ‐induced lung injury and inflammation was assessed. In addition, the in vitro effects and mechanisms of wogonin were studied in the mouse macrophage cell lines Ana‐1 and RAW264.7. In vivo results indicated that wogonin attenuated LPS‐induced histological alterations. Peripheral blood leucocytes decreased in the LPS‐induced group, which was ameliorated by wogonin. In addition, wogonin inhibited the production of several inflammatory cytokines, including tumour necrosis factor‐α, interleukin‐1β (IL‐1β) and IL‐6, in the bronchoalveolar lavage fluid and lung tissues after LPS challenge, while the peroxisome proliferator‐activated receptor γ (PPARγ) inhibitor GW9662 reversed these effects. In vitro results indicated that wogonin significantly decreased the secretion of IL‐6, IL‐1β and tumour necrosis factor‐α in Ana‐1 and RAW264.7 cells, which was suppressed by transfection of PPARγ small interfering RNA and GW9662 treatment. Moreover, wogonin activated PPARγ, induced PPARγ‐mediated attenuation of the nuclear translocation and the DNA‐binding activity of nuclear factor‐κB in vivo and in vitro. In conclusion, all of these results showed that wogonin may serve as a promising agent for the attenuation of ALI‐associated inflammation and pathology by regulating the PPARγ‐involved nuclear factor‐κB pathway. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Immunology Wiley

Wogonin prevents lipopolysaccharide‐induced acute lung injury and inflammation in mice via peroxisome proliferator‐activated receptor gamma‐mediated attenuation of the nuclear factor‐kappaB pathway

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References (70)

Publisher
Wiley
Copyright
"Copyright © 2014 John Wiley & Sons Ltd"
ISSN
0019-2805
eISSN
1365-2567
DOI
10.1111/imm.12305
pmid
24766487
Publisher site
See Article on Publisher Site

Abstract

Acute lung injury (ALI) from a variety of clinical disorders, characterized by diffuse inflammation, is a cause of acute respiratory failure that develops in patients of all ages. Previous studies reported that wogonin, a flavonoid‐like chemical compound which was found in Scutellaria baicalensis, has anti‐inflammatory effects in several inflammation models, but not in ALI. Here, the in vivo protective effect of wogonin in the amelioration of lipopolysaccharide (LPS) ‐induced lung injury and inflammation was assessed. In addition, the in vitro effects and mechanisms of wogonin were studied in the mouse macrophage cell lines Ana‐1 and RAW264.7. In vivo results indicated that wogonin attenuated LPS‐induced histological alterations. Peripheral blood leucocytes decreased in the LPS‐induced group, which was ameliorated by wogonin. In addition, wogonin inhibited the production of several inflammatory cytokines, including tumour necrosis factor‐α, interleukin‐1β (IL‐1β) and IL‐6, in the bronchoalveolar lavage fluid and lung tissues after LPS challenge, while the peroxisome proliferator‐activated receptor γ (PPARγ) inhibitor GW9662 reversed these effects. In vitro results indicated that wogonin significantly decreased the secretion of IL‐6, IL‐1β and tumour necrosis factor‐α in Ana‐1 and RAW264.7 cells, which was suppressed by transfection of PPARγ small interfering RNA and GW9662 treatment. Moreover, wogonin activated PPARγ, induced PPARγ‐mediated attenuation of the nuclear translocation and the DNA‐binding activity of nuclear factor‐κB in vivo and in vitro. In conclusion, all of these results showed that wogonin may serve as a promising agent for the attenuation of ALI‐associated inflammation and pathology by regulating the PPARγ‐involved nuclear factor‐κB pathway.

Journal

ImmunologyWiley

Published: Oct 1, 2014

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