【摘 要】
：
目的：肠三叶因子对胃黏膜具有保护作用,然而其保护机制尚不明确,本研究拟探讨重组肠三叶因子(intestinal trefoil factor, ITF)对胃黏膜上皮细胞增殖能力的影响及其可能作用的分子机制.方法：体外培养GES-1细胞,分别加入浓度为100ng/ml、500ng/ml的人重组ITF,光镜下观察细胞形态.采用CCK-8试剂盒检测GES-1细胞的增殖活力.体外培养的GES-1细胞株,分
【机 构】
：
江苏南京 南京军区南京总医院急救医学科 南京大学医学院附属金陵医院 210002
【出 处】
：
2014北京协和急诊医学国际高峰论坛
论文部分内容阅读
目的：肠三叶因子对胃黏膜具有保护作用,然而其保护机制尚不明确,本研究拟探讨重组肠三叶因子(intestinal trefoil factor, ITF)对胃黏膜上皮细胞增殖能力的影响及其可能作用的分子机制.方法：体外培养GES-1细胞,分别加入浓度为100ng/ml、500ng/ml的人重组ITF,光镜下观察细胞形态.采用CCK-8试剂盒检测GES-1细胞的增殖活力.体外培养的GES-1细胞株,分别用100ng/ml的ITF和PI3K/Akt信号通路抑制剂浓度15μM的LY294002进行处理,实验分组为对照组、LY294002组、ITF组和ITF+LY294002组,光镜下观察细胞形态.随后采用CCK-8试剂盒检测GES-1细胞处理后的增殖活力,采用Western blot检测PI3K/Akt信号通路中p-Akt和Akt蛋白的表达情况.结果：与对照组相比, ITF的刺激下GES-1细胞增殖活力明显增强,且ITF浓度越高、增殖活力越高.使用LY294002处理后,能够显著抑制ITF刺激的细胞增殖.Western blot检测结果说明,ITF提高了p-Akt蛋白的表达水平,其可能通过激活PI3K/Akt信号通路来调控GES-1细胞的增殖,LY294002抑制PI3K/Akt信号通路能够显著抑制GES-1细胞的增殖活力.结论：ITF促进GES-1细胞的增殖,推测其分子作用机制主要是通过激活PI3K/Akt信号通路促进细胞增殖.
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