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Moderate exercise prevents chronic stress induced intestinal barrier dysfunction by promoting hypoxia inducible factor‐1α expression
Author(s) -
Luo Beibei,
Nieman David C.,
Xiang Dao,
Chen Peijie
Publication year - 2013
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.27.1_supplement.lb770
Subject(s) - chromosomal translocation , intestinal permeability , barrier function , in situ hybridization , hypoxia (environmental) , medicine , endocrinology , gene expression , saline , hypoxia inducible factors , placebo , andrology , immunology , biology , chemistry , gene , pathology , biochemistry , microbiology and biotechnology , organic chemistry , oxygen , alternative medicine
Chronic stress induces intestinal barrier dysfunction and impairs mucosal defenses against luminal bacteria. The purpose of this study was to investigate the effect of moderate exercise on intestinal barrier function during chronic stress in a mouse model. Balb/c mice (6 week) were randomized into 5 groups (n=6/group): group C functioned as controls; group R was subjected to 6‐hour per day repeated restraint stress (RRS) for 10 consecutive days; group S received 30 min of swimming prior to RRS; group D was injected with hypoxia inducible factor‐1α (HIF‐1α) stabilizer dimethyloxalylglycine (DMOG) before RRS; group P was injected with saline before RRS as a placebo control. Intestinal tissue was biopsied after the first treatment for analysis of HIF‐1α gene and protein expression. Bacterial translocation was determined by 16s rRNA based fluorescence in situ hybridization. FITC‐dextran was used as a measure of intestinal permeability. Thirty minutes of swimming or DMOG injection before RRS prevented bacterial translocation and maintained intestinal permeability (P<.01). HIF‐1α gene and protein expression were significantly increased after swimming and DMOG treatment (P<.05). In conclusion, moderate exercise prevented chronic stress‐induced intestinal barrier dysfunction in mice, in part due to promoting the expression of transcription factor HIF‐1α. Supported by Grant yjscx2012007 and xsxr2012045

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