实验性溃疡性结肠炎大鼠外周血Th17细胞的变化及黄芪多糖对其的影响

目的：观察实验性溃疡性结肠炎大鼠外周血Th17细胞的变化及黄芪多糖对其的影响。方法：雄性清洁级Wistar大鼠40只,随机分成4组：空白组、模型组、黄芪多糖组、柳氮磺胺砒啶（SASP）组。各组在造模后第3d开始给药,共14 d。给药结束后,腹主动脉取血,离心取血清,ELISA法测定IL-17、TGF-β和IL-23。取距肛门2-10cm处结肠,沿肠黏膜缘剪开肠腔,取病变处组织,进行HE染色。结果：与空白组相比,模型组大鼠血清中IL-17、IL-23、TGF-β含量显著增高（P〈0.05）。与模型组比较,SASP组与黄芪多糖组大鼠血清中IL-17、IL-23、TGF-β含量显著降低（P〈0.05）。与SASP组比较,黄芪多糖组大鼠血清中IL-17、IL-23、TGF-β含量降低（P〈0.05）。结肠病理显示：在各治疗组中,黄芪多糖组黏膜结构最完整、炎症细胞最少。结论：Th17细胞在实验性溃疡性结肠炎大鼠外周血中明显升高,黄芪多糖可能通过调节大鼠血清中IL-23、TGF-β的表达来调节Th17细胞,以减轻肠黏膜炎症损伤。     

Down-regulation of miR-141 in gastric cancer and its involvement in cell growth

Purpose  Human microRNA-141 (miR-141), a member of the miR-200 family, has been reported to be associated with various human malignancies. However, it remains unknown whether miR-141 is involved in the pathogenesis of gastric cancer. Therefore, we examined the expression of miR-141 in gastric cancer tissues and the effect of miR-141 overexpression on cancer cell proliferation. Methods  The expression level of miR-141 in 35 pair-matched gastric neoplastic and adjacent non-neoplastic tissues, and in 5 gastric cancer cell lines were examined by quantitative real-time PCR. The growth of MGC-803 cells transfected with miRNA precursor was examined by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazoliumbromide) assay. Results  MiR-141 was significantly down-regulated in 80% (28/35) of primary gastric cancer tissues compared with pair-matched adjacent non-tumor tissues (P < 0.01). The expression of miR-141 was also found to be substantially reduced in several human gastric cancer cell lines such as MGC-803, HGC-27, SGC-7901 and BGC-823 cells. Overexpression of miR-141 with its precursors significantly inhibited the proliferation of gastric cancer cells. Conclusions  These results suggest that miR-141 may be involved in the development of gastric cancer through its inhibitory effect on cell proliferation. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.