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邻苯二甲酸二(2-乙基己基)酯(DEHP)诱导的佐剂效应在哮喘小鼠模型中通过氧化应激介导。

The adjuvant effect induced by di-(2-ethylhexyl) phthalate (DEHP) is mediated through oxidative stress in a mouse model of asthma.

作者信息

You Huihui, Chen Shaohui, Mao Lin, Li Bing, Yuan Ye, Li Rui, Yang Xu

机构信息

Huibei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan 430079, China.

Huibei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan 430079, China.

出版信息

Food Chem Toxicol. 2014 Sep;71:272-81. doi: 10.1016/j.fct.2014.06.012. Epub 2014 Jun 19.

Abstract

Di-(2-ethylhexyl) phthalate, as the most commonly used plasticizer, is considered to be related to the asthma prevalence. There are studies affirming that the DEHP has an adjuvant effect in the pathogenesis of allergy asthma. Oxidative stress is one possible pathway for DEHP-adjuvant effect. Thus, this study explored whether DEHP could induce adjuvant effect in mouse asthma model via oxidative stress pathway. Male BALB/c mice were randomly divided into six groups: (1) saline group, (2) DEHP group, (3) ovalbumin (OVA) group, (4) DEHP+OVA group, (5) OVA+vitamin E (Vit E) group, (6) DEHP+OVA+Vit E group. The exposure dose of DEHP was 30 mg/kg body weight (bw)/day. After 18 days of the exposure protocol. Reactive oxygen species (ROS), glutathione (GSH) and malonaldehyde (MDA) levels and biomarkers related to asthma model were measured. Collectively, these data indicated higher ROS and MDA levels and lower GSH contents in DEHP+OVA group than that in OVA group, while Vit E, an antioxidant, could restore ROS, MDA and GSH levels to control levels and attenuate the DEHP and/or OVA effects. Our observations suggested that there was a relationship between oxidative stress and the adjuvant effect induced by DEHP in this mouse asthma model.

摘要

邻苯二甲酸二(2-乙基己基)酯作为最常用的增塑剂,被认为与哮喘患病率有关。有研究证实,邻苯二甲酸二(2-乙基己基)酯(DEHP)在过敏性哮喘的发病机制中具有佐剂作用。氧化应激是DEHP发挥佐剂作用的一条可能途径。因此,本研究探讨了DEHP是否能通过氧化应激途径在小鼠哮喘模型中诱导佐剂效应。将雄性BALB/c小鼠随机分为六组:(1)生理盐水组,(2)DEHP组,(3)卵清蛋白(OVA)组,(4)DEHP+OVA组,(5)OVA+维生素E(Vit E)组,(6)DEHP+OVA+Vit E组。DEHP的暴露剂量为30毫克/千克体重(bw)/天。在暴露方案实施18天后,检测活性氧(ROS)、谷胱甘肽(GSH)和丙二醛(MDA)水平以及与哮喘模型相关的生物标志物。总体而言,这些数据表明,DEHP+OVA组的ROS和MDA水平高于OVA组,GSH含量低于OVA组,而抗氧化剂Vit E可将ROS、MDA和GSH水平恢复至对照水平,并减弱DEHP和/或OVA的作用。我们的观察结果表明,在该小鼠哮喘模型中,氧化应激与DEHP诱导的佐剂效应之间存在关联。

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