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Berberine inhibits free fatty acid and LPS‐induced inflammation via modulating ER stress response in macrophages
Author(s) -
Wang Yanyan,
Yan Joanna,
Chen Weidong,
Zhou Huiping
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.654.12
Subject(s) - berberine , unfolded protein response , proinflammatory cytokine , inflammation , nonalcoholic fatty liver disease , steatosis , pharmacology , chemistry , chop , lipopolysaccharide , western blot , tumor necrosis factor alpha , apoptosis , immunology , medicine , endocrinology , biochemistry , fatty liver , disease , gene
Inflammation plays a pivotal role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Berberine (BBR), an isoquinoline alkaloid isolated from many medicinal herbs, has been used to treat various diseases including liver diseases for hundreds of years. Our previous studies have shown that BBR inhibits high fat‐diet‐induced steatosis and inflammation in rat model. However, the underlying molecular mechanisms remain to be identified. This study was to identify the potential mechanism by which BBR inhibits free fatty acid (FFA) and LPS‐induced inflammatory response in mouse macrophages. Methods Mouse RAW2674.1 macrophages were treated with palmitic acid (PA) or LPS or PA+ LPS with or without different concentrations of BBR (0–10 μM) for different periods (0–24h). The mRNA and protein levels of IL‐1β, IL‐6, TNF‐α, MCP‐1, COX‐2, and ER stress genes (CHOP, ATF4, XBP‐1) were detected by real time RT‐PCR, Western blot and ELISA, respectively. Results BBR significantly inhibited PA‐ and LPS‐induced activation of ER stress and expression of proinflammatory cytokines (IL‐1β, IL‐6) and COX‐2. PA/LPS‐mediated activation of ERK1/2 was inhibited by BBR in a dose‐dependent manner. Conclusion BBR inhibits PA/LPS‐induced inflammatory responses through modulating ER stress‐mediated ERK1/2 activation in macrophages. Support or Funding Information This work was supported by VA Merit Award I01BX004033 and 1I01BX001390, VA Career Scientist Award IK6BX004477 and National Institutes of Health Grant R01 DK104893 and R01DK‐057543 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .