Abstract
Ulcerative colitis is an inflammatory bowel disease that affects a large number of people around the world. Galectin-1 is a β-galactoside-binding lectin with a broad range of biological activities. The effects of galectin-1 on dextran sulfate sodium (DSS)-induced ulcerative colitis in vivo is not clear. We investigated the effect of galectin-1 on colon morphology, cell proliferation, oxidative stress, antioxidant system, and proinflammatory/antiinflammatory cytokines in a DSS-induced mouse model of ulcerative colitis. Thirty-two C57BL/6 mice were randomly assigned to one of the four groups: control, acute colitis, galectin-1, and DSS+galectin-1. Controls were treated with phosphate-buffered saline (PBS) for seven days. Acute colitis was induced by 3% DSS in drinking water administered orally for five days. Mice in galectin-1 groups were treated with 1 mg/kg recombinant human galectin-1 in PBS for seven consecutive days. Oral DSS administration resulted in acute colitis by causing histopathological changes; an increase in disease activity index (DAI), lipid peroxidation (malondialdehyde [MDA]), myeloperoxidase (MPO), and tumor necrosis factor (TNF)-α levels; a decrease in body weight, colon length, cell proliferation index, catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities, and GSH and interleukin (IL)-10 levels. The treatment with galectin-1 attenuated DSS-induced acute colitis by reducing DAI, MDA, MPO, and TNF-α levels and by increasing body weight, colon length, cell proliferation, antioxidant enzyme activity, GSH, and IL-10 levels. These findings suggest that galectin-1 has proliferative, antioxidant, antiinflammatory, and cytoprotective effects against DSS-induced ulcerative colitis in mice. Due to its antiinflammatory and antioxidant activity galectin-1 may be effective in preventing and treating ulcerative colitis.
Highlights
Ulcerative colitis is characterized by severe inflammation and ulcer formation in the colon mucosa and submucosa
The body weight of mice in dextran sulfate sodium (DSS)+galectin-1 group significantly increased throughout the experiment from the 4th day compared to DSS group (p < 0.001)
This is consistent with the studies cited above. These results suggest that, in DSS-induced ulcerative colitis model, oxidative stress and lipid peroxidation are increased in the colon tissue, due to the activation of neutrophils and macrophages, while the antioxidant defense system is greatly suppressed
Summary
Ulcerative colitis is characterized by severe inflammation and ulcer formation in the colon mucosa and submucosa. It can be caused by genetic factors or various infectious agents. Ulcerative colitis can be triggered by factors such as smoking, stress, alcohol, and refined foods [1]. Many studies have been carried out to understand the underlying mechanism of ulcerative colitis [2,3], and the potential mechanisms include infiltration of inflammatory cells, activation of T cells, induction of proinflammatory cytokines, and oxidative stress. Submitted: 29 November 2019/Accepted: 29 December 2019
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