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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
Author(s) -
Yao Jing,
Pan Di,
Zhao Yue,
Zhao Li,
Sun Jie,
Wang Yu,
You QiDong,
Xi Tao,
Guo QingLong,
Lu Na
Publication year - 2014
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12305
Subject(s) - peroxisome proliferator activated receptor , inflammation , lipopolysaccharide , wogonin , medicine , receptor , lung , peroxisome , cancer research , immunology , pathology , scutellaria baicalensis , alternative medicine , traditional chinese medicine
Summary 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 RAW 264.7. 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‐1 β ( IL ‐1 β ) and IL ‐6, in the bronchoalveolar lavage fluid and lung tissues after LPS challenge, while the peroxisome proliferator‐activated receptor γ ( PPAR γ ) inhibitor GW 9662 reversed these effects. In vitro results indicated that wogonin significantly decreased the secretion of IL ‐6, IL ‐1 β and tumour necrosis factor‐ α in Ana‐1 and RAW 264.7 cells, which was suppressed by transfection of PPAR γ small interfering RNA and GW 9662 treatment. Moreover, wogonin activated PPAR γ , induced PPAR γ ‐mediated attenuation of the nuclear translocation and the DNA ‐binding activity of nuclear factor‐ κ B 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 PPAR γ ‐involved nuclear factor‐ κ B pathway.