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Eriodictyol ameliorates lipopolysaccharide‐induced acute lung injury by suppressing the inflammatory COX‐2/NLRP3/NF‐κB pathway in mice
Author(s) -
Wang Xia,
Deng Rong,
Dong Junying,
Huang Lu,
Li Junxia,
Zhang Bingqing
Publication year - 2020
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22434
Subject(s) - eriodictyol , malondialdehyde , lipopolysaccharide , bronchoalveolar lavage , tumor necrosis factor alpha , chemistry , myeloperoxidase , pharmacology , superoxide dismutase , nf κb , prostaglandin e2 , inflammation , immunology , signal transduction , medicine , lung , oxidative stress , biochemistry , luteolin , antioxidant , quercetin
The purpose of this paper is to observe the protective action and its effective mechanism of eriodictyol on lipopolysaccharide (LPS)‐induced acute lung injury (ALI). In this study, our results indicated that eriodictyol could dramatically suppress the inflammatory mediators, including interleukin‐6 (IL‐6), IL‐1β, prostaglandin E2, and tumor necrosis factor‐α in bronchoalveolar lavage fluid of LPS‐challenged mice. Eriodictyol also alleviated the wet/dry ratio and improved pathological changes of the lung. In addition, eriodictyol significantly decreased myeloperoxidase activity and malondialdehyde content as well as increased superoxide dismutase activity. Moreover, eriodictyol inhibited the COX‐2/NLRP3/NF‐κB signaling pathway in the lung tissues of ALI mice. In conclusion, our observations validated that eriodictyol processed the protective effects on ALI mice, which was related to the regulation of the COX‐2/NLRP3/NF‐κB signaling pathway.