Galectin-1 reduces the severity of dextran sulfate sodium (DSS)-induced ulcerative colitis by suppressing inflammatory and oxidative stress response
Galectin-1 reduces the severity of dextran sulfate sodium (DSS)-induced ulcerative colitis by suppressing inflammatory and oxidative stress response
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DOI：
10.17305/bjbms.2019.4539
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发表时间：
2020-01-01
影响因子：
3.4
通讯作者：
Aykol-Celik, Guliz
中科院分区：
文献类型：
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作者：
Arda-Pirincci, Pelin;Aykol-Celik, Guliz
溃疡性结肠炎是一种炎症性肠病，影响世界各地许多人。 Galectin-1 是一种 β-半乳糖苷结合凝集素，具有广泛的生物活性。 Galectin-1 对葡聚糖硫酸钠 (DSS) 诱导的体内溃疡性结肠炎的影响尚不清楚。我们在 DSS 诱导的溃疡性结肠炎小鼠模型中研究了 galectin-1 对结肠形态、细胞增殖、氧化应激、抗氧化系统和促炎/抗炎细胞因子的影响。 32 只 C57BL/6 小鼠被随机分配到四组中的一组：对照组、急性结肠炎组、galectin-1 组和 DSS+galectin-1 组。对照组用磷酸盐黄油盐水 (PBS) 处理 7 天。口服 3% DSS 饮用水诱发急性结肠炎 5 天。 Galectin-1组的小鼠用PBS中的1mg/kg重组人Galectin-1连续治疗7天。口服 DSS 引起组织病理学变化，导致急性结肠炎；疾病活动指数 (DAI)、脂质过氧化（丙二醛 MDA]）、髓过氧化物酶 (MPO) 和肿瘤坏死因子 (TNF)-α 水平增加；体重、结肠长度、细胞增殖指数、过氧化氢酶、谷胱甘肽过氧化物酶 (GSH-Px) 和超氧化物歧化酶 (SOD) 活性以及 GSH 和白细胞介素 (IL)-10 水平下降。 Galectin-1 治疗通过降低 DAI、MDA、MPO 和 TNF-α 水平以及增加体重、结肠长度、细胞增殖、抗氧化酶活性、GSH 和 IL-10 水平来减轻 DSS 诱导的急性结肠炎。这些发现表明，galectin-1 对 DSS 诱导的小鼠溃疡性结肠炎具有增殖、抗氧化、抗炎和细胞保护作用。由于其抗炎和抗氧化活性，半乳糖凝集素-1 可有效预防和治疗溃疡性结肠炎。
Ulcerative colitis is an inflammatory bowel disease that affects a large number of people around the world. Galectin-1 is a beta-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-buttered 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)-alpha 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 DSSinduced acute colitis by reducing DAI, MDA, MPO, and TNF-alpha 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.