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Ethanol‐induced ROS production is prevented by globular adiponectin via modulation of Nox2 expression in macrophages (844.19)
Author(s) -
Kim Mijin,
Nepal Saroj,
Shrestha Anup,
TiliJa pun Nirmala,
Park PilHoon
Publication year - 2014
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.28.1_supplement.844.19
Subject(s) - nadph oxidase , adiponectin , nox4 , chemistry , microbiology and biotechnology , reactive oxygen species , stimulation , oxidase test , biochemistry , enzyme , biology , endocrinology , insulin resistance , insulin
Adiponectin predominantly secreted from adipose tissue plays a crucial role in lipid metabolism and possesses potent anti‐inflammatory properties. Adipoonectin has been shown to generate protective effects in a number of pathophysiological states. Recently, it has been shown that adiponectin prevents ROS production induced by stimulation with various stimuli. In the present study, we investigated the effect of globular adiponectin (gAcrp) on ethanol‐induced ROS production in macrophages and underlying mechanisms. Herein, we found that gAcrp efficiently suppresses ethanol‐induced ROS production both in RAW 264.7 macrophages and murine peritoneal macrophages. We next investigated the role of NADPH oxidase, comprising a multi‐component enzyme complex, in the suppression of ROS production by gAcrp, since NADPH oxidase plays a critical role in ethanol‐induced ROS production in macrophages. Globular adiponectin prevented ethanol‐induced NAPDH oxidase activation. Particularly, it inhibited ethanol‐induced increase in expression of Nox2 and p22 phox . Furthermore, gAcrp restored ethanol‐induced activation of p38MAPK‐NF‐κB pathway, which is critical for Nox2 expression. Taken together, these results suggest that adiponectin prevents ethanol‐induced ROS production via modulation of NADPH oxidase in macrophages.