Swimming attenuates inflammation, oxidative stress, and apoptosis in a rat model of dextran sulfate sodium-induced chronic colitis

// Ling Qin 1,* , Zhi-qiang Yao 2,* , Qi Chang 3,* , Ya-li Zhao 2,* , Ning-ning Liu 2,* , Xiao-shan Zhu 2 , Qin-qin Liu 2 , Li-feng Wang 4 , An-gang Yang 5 , Chun-fang Gao 2 and Jun-tang Li 2,3,4,5 1 Department of Hematology, First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, Henan, China 2 Centre of Inflammation and Cancer Research, 150th Central Hospital of PLA, Luoyang, Henan, China 3 Centre of Biomaterial and Biophysics Research, Institute of Training Medicine, 150th Central Hospital of PLA, Luoyang, Henan, China 4 State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi’an, Shaanxi, China 5 State Key Laboratory of Cancer Biology, Department of Immunology, Fourth Military Medical University, Xi’an, Shaanxi, China * These authors have contributed equally to this work Correspondence to: Jun-tang Li, email: // Chun-fang Gao, email: // Ling Qin, email: // Keywords : chronic colitis, swimming, inflammation, oxidative stress, apoptosis, Immunology and Microbiology Section, Immune response, Immunity Received : March 28, 2016 Accepted : December 15, 2016 Published : December 21, 2016 Abstract Increasing evidence suggests that regular physical exercise suppresses chronic inflammation. However, the potential inhibitory effects of swimming on dextran sulfate sodium (DSS)-induced chronic colitis, and its underlying mechanisms, remain unclear. In this study, rats were orally administered DSS to induce chronic colitis, and subsequently treated with or without swimming exercise. A 7-week swimming program (1 or 1.5 hours per day, 5 days per week) ameliorated DSS-caused colon shortening, colon barrier disruption, spleen enlargement, serum LDH release, and reduction of body weight gain. Swimming for 1.5 hours per day afforded greater protection than 1 hour per day. Swimming ameliorated DSS-induced decrease in crypt depth, and increases in myeloperoxidase activity, infiltration of Ly6G + neutrophils and TNF-α- and IFN-γ-expressing CD3 + T cells, as well as fecal calprotectin and lactoferrin. Swimming inhibited pro-inflammatory cytokine and chemokine production and decreased the protein expression of phosphorylated nuclear factor-κB p65 and cyclooxygenase 2, whereas it elevated interleukin-10 levels. Swimming impeded the generation of reactive oxygen species, malondialdehyde, and nitric oxide; however, it boosted glutathione levels, total antioxidant capacity, and superoxide dismutase and glutathione peroxidase activities. Additionally, swimming decreased caspase-3 activity and expression of apoptosis-inducing factor, cytochrome c, Bax, and cleaved-caspase-3, but increased Bcl-2 levels. Overall, these results suggest that swimming exerts beneficial effects on DSS-induced chronic colitis by modulating inflammation, oxidative stress, and apoptosis.