首页> 中文期刊> 《海南医学院学报》 >脓毒症患儿Treg/Th17失衡与全身炎症反应、氧化应激所致肝损伤的相关性

脓毒症患儿Treg/Th17失衡与全身炎症反应、氧化应激所致肝损伤的相关性

         

摘要

目的:研究脓毒症患儿Treg/Th17失衡与全身炎症反应、氧化应激所致肝损伤的相关性.方法:选择在本院诊断为脓毒症的43例患儿作为研究的脓毒症组,同期在上海市嘉定区中心医院门诊健康体检的35例儿童作为研究的对照组.采集外周血并测定Treg、Th17的含量以及氧化应激分子的表达量,采集血清并测定炎症反应分子、氧化应激分子、肝损伤指标的含量.结果:脓毒症组患儿外周血中Treg、Th17的含量以及Treg/Th17的比例均显著高于对照组;脓毒症组患儿血清中ALT、AST、TBIL、γ-GT、MIF、sTREM-1、sVCAM-1、PCT的含量以及外周血中MPO、Nrf-2的mRNA表达量显著高于对照组且与外周血中Treg/Th17的比例呈正相关,外周血中Keap-1的mRNA表达量以及血清中SOD、GSH的含量均显著低于对照组且与外周血中Treg/Th17的比例呈负相关.结论:脓毒症患儿外周血中Treg/Th17比例升高与全身炎症反应及氧化应激反应的激活、肝功能的损伤密切相关.%Objective:To study the correlation between Treg/Th17 imbalance and the liver injury caused by systemic inflammatory response and oxidative stress in children with sepsis.Methods:43 children who were diagnosed with sepsis in Shanghai Jiading District Central Hospital between February 2016 and March 2017were selected as the sepsis group of the study,and children who received physical examination in Outpatient Clinic of Shanghai Jiading District Central Hospital during the same period were selected as the control group of the study.The peripheral blood was collected to determine the contents of Treg and Th17 as well as the expression of oxidative stress molecules,and serum was collected to determine the contents of inflammatory reaction molecules,oxidative stress molecules and liver injury indexes.Results:Peripheral blood Treg and Th17 contents as well as Treg/Th17 of sepsis group were significantly higher than those of control group;serum ALT,AST,TBIL,γ-GT,MIF,sTREM-1,sVCAM-1 and PCT contents as well as peripheral blood MPO and Nrf-2 mRNA expression of sepsis group were significantly higher than those of control group and positively correlated with peripheral blood Treg/Th17 while peripheral blood Keap-1 mRNA expression as well as serum SOD and GSH contents was significantly lower than that of control group and negatively correlated with peripheral blood Treg/Th17.Conclusion:The increase of Treg/Th17 in peripheral blood of children with sepsis is closely related to the activation of inflammatory response and oxidative stress response and the injury of liver function.

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