研究报告

  • 雷璠,李崇尧,彭旗,王曼,唐帆,姚蕾,吴永亮,敖紫淳,马萍.内质网应激和氧化应激通路对DINP诱发Allergic March的介导作用[J].环境科学学报,2020,40(11):4199-4206

  • 内质网应激和氧化应激通路对DINP诱发Allergic March的介导作用
  • Mediating effect of endoplasmic reticulum stress and oxidative stress pathways on allergic march induced by DINP
  • 基金项目:湖北省高等学校优秀中青年科技创新团队计划项目(No.T201717);咸宁市科技计划项目(No.2019KJ11)
  • 作者
  • 单位
  • 雷璠
  • 湖北科技学院药学院, 咸宁 437100
  • 李崇尧
  • 湖北科技学院药学院, 咸宁 437100
  • 彭旗
  • 湖北科技学院药学院, 咸宁 437100
  • 王曼
  • 湖北科技学院基础医学院, 环境-免疫与神经系统疾病实验室, 咸宁 437100
  • 唐帆
  • 湖北科技学院基础医学院, 环境-免疫与神经系统疾病实验室, 咸宁 437100
  • 姚蕾
  • 湖北科技学院基础医学院, 环境-免疫与神经系统疾病实验室, 咸宁 437100
  • 吴永亮
  • 湖北科技学院基础医学院, 环境-免疫与神经系统疾病实验室, 咸宁 437100
  • 敖紫淳
  • 湖北科技学院基础医学院, 环境-免疫与神经系统疾病实验室, 咸宁 437100
  • 马萍
  • 湖北科技学院基础医学院, 环境-免疫与神经系统疾病实验室, 咸宁 437100
  • 摘要:为了研究增塑剂邻苯二甲酸二异壬酯(diisononyl phthalate,DINP)致Allergic March的作用机制,以雄性BALB/c小鼠为受试动物,随机分为5组,包括空白对照组(生理盐水)、20 mg·kg-1 DINP组、OVA组、20 mg·kg-1 DINP+OVA组和4-苯基丁酸(4-PBA)拮抗组(20 mg·kg-1 DINP+OVA+4-PBA),染毒周期为47 d.以肺组织匀浆测定活性氧(reactive oxygen species,ROS)、还原型谷胱甘肽(glutathione,GSH)、丙二醛(malondialdehyde,MDA)和一氧化氮(nitric oxide,NO).采用ELISA试剂盒检测血清中总免疫球蛋白E(T-IgE)、OVA特异性免疫球蛋白E(OVA-IgE)和白细胞介素-33(IL-33)评价机体的炎症因子,并同时观察肺组织的病理变化结果.与生理盐水组比较,OVA组的肺功能、Th2免疫系统功能亢进的分子、氧化应激指标和肺组织病理学损伤都有所加重.与OVA组比较,20 mg·kg-1 DINP+OVA组的肺功能、Th2免疫系统功能亢进的分子、氧化应激指标和肺组织病理学损伤同样也有所加重.而4-PBA拮抗组(20 mg·kg-1 DINP+OVA+4-PBA)与20 mg·kg-1 DINP+OVA组相比较,其各项指标都有了明显的减轻.实验结果表明,20 mg·kg-1的DINP能加重小鼠的Allergic March,内质网应激拮抗剂4-PBA可使Allergic March症状减轻,对小鼠肺组织起保护作用,说明内质网应激通路可能通过调节氧化应激介导了DINP所致的Allergic March.
  • Abstract:In order to investigate the action mechanism of plasticizer diisononyl phthalate (DINP) on Allergic March. Male BALB/c mice were randomly divided into 5 groups, including blank control group (normal saline), 20 mg·kg-1 DINP group, OVA group, 20 mg·kg-1 DINP + OVA group, and 4-PBA antagonist group (20 mg·kg-1 DINP + OVA + 4-PBA), with a exposure period of 47 days. Lung tissue homogenate was used to measure reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and nitric oxide (NO). ELISA kits were used to detect T-IgE, OVA-IgE and IL-33 in serum to evaluate the body's inflammatory factors, and at the same time to observe the results of lung tissue pathological changes. Compared with the saline group, lung function, molecules of Th2 immune system hyperfunction, indicators of oxidative stress, and lung histopathological damage all increased in the OVA group. Compared with the OVA group, the 20 mg·kg-1 DINP + OVA group also exacerbated lung function, molecules of Th2 immune system hyperfunction, oxidative stress indicators and lung histopathological damage. However, compared with the 20 mg·kg-1 DINP + OVA group, the 4-PBA antagonist group, its indicators were significantly reduced. The experimental results show that 20 mg·kg-1 of DINP can aggravates Allergic March in mice. Endoplasmic reticulum stress antagonist 4-PBA can reduce the symptoms of Allergic March and protect the lung tissue of mice, and it is demonstrated that the endoplasmic reticulum stress pathway may mediates the allergic march induced by DINP via regulating oxidative stress.

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