论文部分内容阅读
目的研究微小RNA-126(micro RNA-126,miR-126)基因敲减(knock down,KD)对CD4~+T细胞介导的自身免疫性结肠炎模型的影响并探讨其意义。方法常规利用DSS溶液喂养野生型(WT)和miR-126基因敲减(miR-126KD)小鼠,诱导急性自身免疫性结肠炎模型。HE染色观察小鼠结肠组织病理变化;FACS检测CD4~+T细胞的比例变化及其表面活化分子CD62L、CD44的表达;MACS分选出WT和miR-126KD小鼠脾脏中CD4~+CD62L+T细胞,CFSE染色标记后,分别经尾静脉转输给WT小鼠,再诱导自身免疫性结肠炎模型;HE染色观察结肠组织病理变化;FACS检测CFSE阳性CD4~+T细胞表面活化分子CD62L、CD44的表达变化。结果与对照组相比,miR-126KD小鼠肠组织绒毛缺失不完整,黏膜上皮出现较大溃疡,炎性细胞浸润增加;FACS结果显示,miR-126KD组小鼠CD4~+T细胞比例和总数显著上调(P<0.01);且高表达CD44,低表达CD62L;过继转输实验结果显示,miR-126KD小鼠CD4~+T细胞转输组结肠组织损伤加重;同时,CFSE+细胞高表达CD44,低表达CD62L。结论 miR-126基因敲减加重葡聚糖硫酸钠所致肠炎的病变程度。
Objective To investigate the effect of microRNA-126 (miR-126) knockdown (KD) on CD4 ~ + T cell-mediated autoimmune colitis in rats and its significance. Methods Wild type (WT) and miR-126 knockdown (miR-126KD) mice were routinely administered with DSS solution to induce acute autoimmune colitis. The histopathological changes of colonic tissue were observed by HE staining. The proportion of CD4 ~ + T cells and the expression of CD62L and CD44 were detected by FACS. The percentage of CD4 ~ + CD62L + T The cells were stained with CFSE and then transfused into WT mice respectively via tail vein to induce the model of autoimmune colitis. The histopathological changes of colon were observed by HE staining. The expressions of CD62L, CD44 Changes in expression. Results Compared with the control group, the deletion of villus in miR-126KD mice was incomplete and the mucosal epithelium showed larger ulceration and inflammatory cell infiltration. Compared with the control group, the percentage of CD4 ~ + T cells in miR-126KD group and the total number (P <0.01). The results of adoptive transfer showed that the injury of colon tissue of CD4 ~ + T cells in miR-126KD mice was increased. At the same time, CFSE + cells highly expressed CD44, Low expression of CD62L. Conclusions The miR-126 gene knockdown aggravates the severity of enteritis induced by dextran sodium sulfate.