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OBJECTIVE Although it is generally believed that nicotine accounts for the beneficial effect of smoking on ulcerative colitis, the underlying mechanisms remain not well- understood. Our previous finding that nicotine inhibits inflammatory responses through inducing miRNA-124 prompted us to ask whether the miRNA is involved in the protective action of nicotine on UC. METHODS MiR-124 expression in colon tissues and cells was determined by q-PCR and in situ hybridization. The effect of miR-124 on protective role of nicotine in ulcerative colitis was evaluated in DSS-treated mice and IL-6-treated Caco-2 colon epithelial cells. Expression of p-STAT3/STAT3 was detected by immuno?histochemistry and Western blot analysis. RESULTS miR- 124 expression is upregulated in colon tissues from patients and DSS- induced colitis. Nicotine treatment further elevated miR- 124 level in colon tissues of the mice, in infiltrated lymphocytes and epithelial cells, and augmented miR- 124 expression in lymphocytes isolated from

来源:中国药理学与毒理学杂志 2017 年 31卷 10期

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中国药理学与毒理学杂志 2017 年 31卷 10期
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microRNA- 124 nicotine ulcerative colitis p- STAT3 human T lymphocytes colon epithelial cell
OBJECTIVE Although it is generally believed that nicotine accounts for the beneficial effect of smoking on ulcerative colitis, the underlying mechanisms remain not well- understood. Our previous finding that nicotine inhibits inflammatory responses through inducing miRNA-124 prompted us to ask whether the miRNA is involved in the protective action of nicotine on UC. METHODS MiR-124 expression in colon tissues and cells was determined by q-PCR and in situ hybridization. The effect of miR-124 on protective role of nicotine in ulcerative colitis was evaluated in DSS-treated mice and IL-6-treated Caco-2 colon epithelial cells. Expression of p-STAT3/STAT3 was detected by immuno?histochemistry and Western blot analysis. RESULTS miR- 124 expression is upregulated in colon tissues from patients and DSS- induced colitis. Nicotine treatment further elevated miR- 124 level in colon tissues of the mice, in infiltrated lymphocytes and epithelial cells, and augmented miR- 124 expression in lymphocytes isolated from