nicotineulcerativecolitiscolonepithelialcell
摘要：A large body of epidemiological and clinical evidences indicated that smoking has a protective effect in patients with ulcerative colitis （UC）. Although it is generally believed that nicotine accounts for the beneficial effect of smoking on UC, the underlying mechanism remains largely unknown. Our previously investigations demon- strated that nicotine inhibits inflammatory responses via inducing miRNA-124, which prompted us to ask whether miR-124 is involved in the protective effect of nicotine on UC. We found in the present study that nicotine elevated the level of miR-124 in epithelial colon cancer cell HT-29. MiR-124 overexpression decreased LPS-triggered STAT3 phosphorylation and STAT3 upregulation, whereas its knockdown enhanced LPS-induced p-STAT3/STAT3 increase. In mice UC model, nicotine treatment reduced weight loss, improved disease activity index, decreased HE score and increased miR-124 expression in colon tissues. Furthermore, miR-124 knockdown markedly dimin- ished the beneficial effect of nicotine in UC mice, and attenuated the inhibitory role of nicotine on the STAT3 /p- STAT3 expression in colon tissues. Consistent with its involvement in UC, biopsies samples from patients with UC also contained increased level of miR-124 when compared with that from normal individuals. These data showed that miR-124 is involved in UC and mediates the protective effects of nicotine, suggesting that the mitl-124/STAT3 is a potential target for the therapeutic intervention of UC.
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