山东医药2019，Vol.59Issue(5)：44-46,3.DOI:10.3969/j.issn.1002-266X.2019.05.012
激活Notch信号通路对人滋养细胞氧化应激损伤的影响及机制
Effect of Notch signaling pathway on oxidative stress in human trophoblast cells
摘要
Abstract
Objective To investigate the role of Notch signaling pathway in oxidative stress of human trophoblast cells of preeclampsia and its mechanism. Methods HTR8/SVneo cells were divided into the normal control group, hypoxia/reoxygenation (H/R) treatment group, and recombinant human neurotrophic factor (rh NF) -κB + H/R treatment group.The normal control group was cultured routinely; the H/R group was cultured under hypoxia for 8 h, followed by routine culture for 16 h, two cycles for 48 h; the rh NF-κB + H/R group was first incubated with 1 gsu/m L the NOTCH signal pathway activator rh NF-κB for 2 h, and then treated with H/R. Flow cytometry was used to detect the apoptotic rate and reactive oxygen species (ROS) level. Western blotting was used to detect the expression of Notch1, hes1, soluble vascular endothelial growth factor receptor (s Flt) -1, and vascular endothelial growth factor (VEGF) in each group. Results The apoptotic rate, ROS level, s Flt-1, and VEGF protein expression in the H/R group were higher than those in the normal control group, while the protein expression of Notch1 and Hes1 was lower than that in the normal control group (all P <0.01); the apoptotic rate, ROS level, s Flt-1, and VEGF protein expression in the rh NF-κB + H/R group were lower than those in the H/R group, while the protein expression of Notch1 and Hes1 was higher than that in the H/R group (all P <0.01). Conclusions Activation of Notch signaling pathway can reduce the apoptosis of trophoblast cells induced by oxidative stress, and its mechanism may be related to the decrease of ROS level, s Flt-1, and the VEGF expression.关键词
子痫前期/Notch信号通路/滋养层细胞/氧化应激损伤Key words
preeclampsia/Notch1 signaling pathway/trophoblast cells/oxidative stress injury分类
医药卫生引用本文复制引用
任艳芳,姜永杰,张秀玲,姜姗,王玉红..激活Notch信号通路对人滋养细胞氧化应激损伤的影响及机制[J].山东医药,2019,59(5):44-46,3.基金项目
河南省高等学校重点科研计划项目(17A320002) （17A320002）
