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Atractylodin attenuates the expression of MUC5AC and extracellular matrix in lipopolysaccharide‐induced airway inflammation by inhibiting the NF‐κB pathway
Author(s) -
Dong Yanpeng,
Zhang Xiao,
Yao Chuan,
Xu Rui,
Tian Xiaohong
Publication year - 2021
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.23311
Subject(s) - lipopolysaccharide , ovalbumin , inflammation , mucin , chemistry , blot , microbiology and biotechnology , nf κb , extracellular matrix , immunology , biology , biochemistry , immune system , gene
This study aimed to explore the effects of atractylodin (ATR) on lipopolysaccharide (LPS)‐induced inflammatory response in human airway epithelial cells. The cytotoxicity was assessed by CCK‐8 assay. The mRNA expression and concentration of interleukin (IL)‐6, IL‐8, and mucin 5AC (MUC5AC) were measured by qRT‐PCR and ELISA, respectively. Western blotting was performed to determine protein expression. We found that LPS stimulation increased the mRNA expression and concentrations of IL‐6, IL‐8, and MUC5AC, as well as the expression of Col‐I and FN in 16HBE cells, but this effect of LPS was attenuated by ATR treatment. Mechanistically, ATR suppressed LPS‐induced activation of the NF‐κB pathway in 16HBE cells. Moreover, ATR repressed ovalbumin‐induced airway inflammation and NF‐kB pathway in mice. In conclusion, ATR attenuated the expression of MUC5AC and ECM in LPS‐induced airway inflammation by inhibiting the NF‐κB pathway.