TNIP2对脂多糖诱导的子宫内膜炎中细胞氧化应激的分子机制研究  

The Molecular Mechanism of TNIP2 on Cellular Oxidative Stress in Lipopolysaccharide-induced Endometritis

作　　者：钱鑫鑫 王妍 李丽萍 李跃文 李兴媚 QIAN Xinxin;WANG Yan;LI Liping;LI Yuewen;LI Xingmei(Department of Gynecology,Section Two,The Third Affiliated Hospital of Qiqihar Medical University,Qiqihar 161000,Heilongjiang,China;Department of Obstetrics,The Third Affiliated Hospital of Qiqihar Medical University,Qiqihar 161000,Heilongjiang,China)

机构地区：[1]齐齐哈尔医学院附属第三医院妇二科,黑龙江齐齐哈尔161000 [2]齐齐哈尔医学院附属第三医院产科,黑龙江齐齐哈尔161000

出　　处：《系统医学》2025年第5期1-7,共7页Systems Medicine

基　　金：2022年度黑龙江省省属高等学校基本科研业务费科研项目(2022-KYYWF-0801)。

摘　　要：目的本研究旨在利用脂多糖(lipopolysaccharide,LPS)刺激人子宫内膜上皮细胞(human endometrial epithelial cells,hEEC),构建细胞模型,并探讨肿瘤坏死因子α诱导蛋白3相互作用蛋白2(tumor necrosis factor alpha induced protein 3 interacting protein 2,TNIP2)在子宫内膜炎氧化应激过程中的作用及其潜在机制。方法用LPS诱导hEEC建立子宫内膜炎的细胞模型。通过ELISA检测模型建立效果。使用实时荧光定量反转录聚合酶链反应(real time quantitative PCR,RT-qPCR)检测TNIP2 mRNA水平。建立TNIP2过表达和抑制的基因表达hEEC细胞株,使用RT-qPCR测量TNIP2 mRNA水平,以验证载体构建效果。使用相应的试剂盒测定活性氧(reactive oxygen species,ROS)、超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)水平。通过生物信息学分析TNIP2靶分子及通路。通过MTT检测细胞活性。结果TNIP2表达在由LPS构建的子宫内膜炎模型中下降。在LPS诱导的hEEC中,MDA活性和ROS浓度上调,SOD水平下降。而上调的MDA和ROS;和下调的SOD可以被TNIP2的过表达所逆转。此外,研究发现肿瘤坏死因子(tumor necrosis factor,TNF)通路参与了TNIP2对LPS诱导的子宫内膜炎细胞的氧化应激,TNF通路的激活逆转了TNIP2对LPS诱导的子宫内膜上皮细胞氧化应激的保护作用。结论TNIP2通过抑制TNF通路降低子宫内膜炎细胞的氧化应激。Objective The aim of this study was to use lipopolysaccharide(LPS)to stimulate human endometrial epithelial cells(hEEC)to construct a cell model.To explore the role of tumor necrosis factor alpha induced protein 3 interacting protein 2(TNIP2)in the oxidative stress process of endometritis and its potential mechanism.Methods The cell model of endometritis was established by LPS-induced hEEC.The effect of the model was detected by ELISA.The mRNA level of TNIP2 was detected by real time quantitative PCR(RT-qPCR).The hEEC cell lines with TNIP2 overexpression and inhibition were established,and the level of TNIP2 mRNA was measured by RT-qPCR to verify the effect of vector construction.The levels of reactive oxygen species(ROS),superoxide dismutase(SOD)and malondialdehyde(MDA)were measured by corresponding kits.Bioinformatics analysis of TNIP2 target molecules and pathways.Cell activity was detected by MTT.Results The expression of TNIP2 was decreased in the endometritis model constructed by LPS.In LPS-induced hEEC,MDA activity and ROS concentration were up-regulated,and SOD level was decreased.The up-regulated MDA and ROS and down-regulated SOD can be reversed by overexpression of TNIP2.In addition,the study found that the tumor necrosis factor(TNF)pathway was involved in the oxidative stress of TNIP2 on LPS-induced endometrial inflammatory cells,and the activation of the TNF pathway reversed the protective effect of TNIP2 on LPS-induced oxidative stress in endometrial epithelial cells.Conclusion TNIP2 reduces oxidative stress in endometritis cells by inhibiting the TNF pathway.

关 键 词：子宫内膜炎 肿瘤坏死因子 氧化应激 肿瘤坏死因子α诱导的蛋白3相互作用蛋白2 

分 类 号：R4[医药卫生—临床医学]