Objective To dynamic monitoring the changes of serum cortisol,adrenocorticotropic hormone (ACTH) in children with sepsis and servere sepsis,and to assess it's relationship with clinical features.Methods Thirty children with sepsis were enrolled in this study from Sep 2010 to Jan 2011 in our hospital,and were divided into severe sepsis group (n =10) and sepsis group (n =20).The serum cortisol and ACTH were analysed in acute and recovery period respectively in both two groups,and compared with 10 non-sepsis children as control group.Results In the acute period,the level of serum cortisol in severe sepsis group [ (33.97 ±6.83) μg/ml ] was significantly higher than those in sepsis group [ (26.30 ± 10.43) μg/ml]and control group [ ( 19.06 ± 6.91 ) μg/ml ] ( P ＜ 0.01 ) ; the level of serum ACTH in severe sepsis group [ (25.47 ± 9.41 ) pg/ml ] was significantly higher than those in sepsis group [ ( 15.52 ± 5.85 ) pg/ml ] and control group [ (9.16 ± 3.02 ) pg/ml ] ( P ＜ 0.01 ).Conclusion Stress response exists in the early period of sepsis,and the levels of serum cortisol and ACTH are increased significantly.The levels of serum cortisol and ACTH are positive correlation with the severity of diseases,and they could be used as serious index and a marker for evaluating prognosis in children with sepsis.

[摘 要] 目的：探讨2',4'-二羟基查尔酮（D2）通过调控miR-7-5p诱导自噬，抑制结直肠癌细胞增殖、迁移及上皮间质转化（EMT）的分子机制。方法：选取结直肠癌细胞系HCT-15、SW620为研究对象，分别用不同浓度（0、12.5、25、50 µmol/L）的D2处理细胞，采用MTT法和平板克隆实验检测细胞增殖活力及克隆形成能力，划痕愈合实验及Transwell实验评估细胞迁移能力，WB法检测EMT相关蛋白、自噬相关蛋白及PI3K/AKT/mTOR信号通路蛋白的表达情况，免疫荧光染色法观察自噬小体的形成。基于TCGA数据库分析miR-7-5p在结直肠癌中的表达水平，并借助KEGG富集分析探究miR-7-5p与结直肠癌的关联。运用RT-qPCR检测miR-7-5p的表达量，同时采用慢病毒转染技术构建miR-7-5p稳定敲低或过表达的细胞系。结果：D2抑制结直肠癌细胞的增殖、迁移及EMT进程（P < 0.05或P < 0.01）。TCGA数据库分析及KEGG富集分析显示，miR-7-5p在结直肠癌中呈低表达，且与结直肠癌的发生有密切关联。12.5、25、50 µmol/L D2处理均可上调HCT-15、SW620细胞miR-7-5p的表达水平（均P < 0.01）。25 µmol/L D2处理组HCT-15、SW620细胞中 LC3、p-ULK1等自噬相关蛋白表达增加，而PI3K/AKT/mTOR信号通路受到抑制（均P < 0.05），细胞内自噬小体数量增加（均P < 0.01）；与D2单独处理组相比，经 D2处理的miR-7-5p敲减细胞中LC3、p-ULK表达量有所下降（P < 0.05或P < 0.01）。结论：D2通过调控miR-7-5p诱导自噬，抑制结直肠癌细胞的增殖、迁移及EMT进程，其机制可能与抑制PI3K/AKT/mTOR信号通路有关。