臭氧暴露诱发小鼠急性肺部损伤及抗氧化剂的拮抗作用

郑子龙, 陈雨珊, 杨旭, 曾燕, 李金泉. 臭氧暴露诱发小鼠急性肺部损伤及抗氧化剂的拮抗作用[J]. 生态毒理学报, 2020, 15(6): 151-157. doi: 10.7524/AJE.1673-5897.20200815011
引用本文: 郑子龙, 陈雨珊, 杨旭, 曾燕, 李金泉. 臭氧暴露诱发小鼠急性肺部损伤及抗氧化剂的拮抗作用[J]. 生态毒理学报, 2020, 15(6): 151-157. doi: 10.7524/AJE.1673-5897.20200815011
Zheng Zilong, Chen Yushan, Yang Xu, Zeng Yan, Li Jinquan. Acute Exposure of Ozone Induced Pulmonary Injury in Mice and the Antagonism of Antioxidant[J]. Asian Journal of Ecotoxicology, 2020, 15(6): 151-157. doi: 10.7524/AJE.1673-5897.20200815011
Citation: Zheng Zilong, Chen Yushan, Yang Xu, Zeng Yan, Li Jinquan. Acute Exposure of Ozone Induced Pulmonary Injury in Mice and the Antagonism of Antioxidant[J]. Asian Journal of Ecotoxicology, 2020, 15(6): 151-157. doi: 10.7524/AJE.1673-5897.20200815011

臭氧暴露诱发小鼠急性肺部损伤及抗氧化剂的拮抗作用

    作者简介: 郑子龙(2000-),男,本科生,研究方向为生态毒理学,E-mail:1183112281@qq.com
    通讯作者: 李金泉, E-mail: ljq0615@live.cn
  • 基金项目:

    国家自然科学基金青年基金资助项目(81903278);湖北省教育厅科学研究计划中青年人才项目(Q20191103);武汉科技大学大学生创新创业训练计划项目(20ZA066)

  • 中图分类号: X171.5

Acute Exposure of Ozone Induced Pulmonary Injury in Mice and the Antagonism of Antioxidant

    Corresponding author: Li Jinquan, ljq0615@live.cn
  • Fund Project:
  • 摘要: 为了研究臭氧(ozone,O3)诱发小鼠肺损伤的作用以及褪黑素(melatonin,MT)的保护机制,本研究以雄性Balb/c小鼠为受试动物,进行连续7 d、每天3 h的急性O3暴露,在保护组每天口服暴露5 mg·kg-1 MT。实验小鼠随机分为4组:(1)生理盐水对照组(Control);(2)褪黑素对照组(MT);(3)臭氧暴露组(2.14 mg·m-3 O3);(4)臭氧暴露+褪黑素保护组(2.14 mg·m-3 O3+MT)。最后一次臭氧暴露后,制备小鼠肺泡灌洗液,采用酶联免疫吸附法(ELISA)检测肺组织中IL-1β、IL-33、IL-4和IL-17A的含量;取部分肺组织制作肺匀浆并提取总mRNA,用于检测肺组织中丙二醛(MDA)和还原型谷胱甘肽(GSH)的含量,以及核因子E2相关因子2(Nrf2)、血红素加氧酶1(HO-1)、NADPH:醌氧化还原酶1(NQO-1)mRNA的表达。此外,采用苏木精-伊红染色(H&E stain)观察小鼠肺组织病理学改变。结果表明,与对照组相比,2.14 mg·m-3 O3暴露组小鼠肺组织MDA含量上升,IL-1β、IL-33、IL-4和IL-17A表达增加;GSH含量以及Nrf2HO-1NQO-1的mRNA相对表达量下降,且差异具有统计学意义(P<0.05或P<0.01)。与O3暴露组相比,MT保护组小鼠肺组织MDA含量下降,IL-1β、IL-33、IL-4和IL-17A表达下降,且GSH含量以及Nrf2HO-1NQO-1的mRNA相对表达量相应上升。此外,小鼠肺组织病理切片观察结果表明,O3暴露组小鼠肺组织出现炎细胞浸润和气道重塑现象,使用抗氧化剂MT处理后可减轻相应病理学改变。综上所述,2.14 mg·m-3 O3暴露可造成小鼠肺组织氧化损伤,诱发炎症,导致肺组织病理学改变;抗氧化剂的使用可增加Nrf2及其下游抗氧化酶的表达,缓解氧化应激,降低炎症因子水平,这验证了O3暴露引起的肺部损伤是通过氧化性损伤机制介导的。
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  • 收稿日期:  2020-08-15

臭氧暴露诱发小鼠急性肺部损伤及抗氧化剂的拮抗作用

    通讯作者: 李金泉, E-mail: ljq0615@live.cn
    作者简介: 郑子龙(2000-),男,本科生,研究方向为生态毒理学,E-mail:1183112281@qq.com
  • 1. 武汉科技大学医学院, 脑科学先进技术研究院, 武汉 430081;
  • 2. 华中师范大学生命科学学院, 武汉 430079
基金项目:

国家自然科学基金青年基金资助项目(81903278);湖北省教育厅科学研究计划中青年人才项目(Q20191103);武汉科技大学大学生创新创业训练计划项目(20ZA066)

摘要: 为了研究臭氧(ozone,O3)诱发小鼠肺损伤的作用以及褪黑素(melatonin,MT)的保护机制,本研究以雄性Balb/c小鼠为受试动物,进行连续7 d、每天3 h的急性O3暴露,在保护组每天口服暴露5 mg·kg-1 MT。实验小鼠随机分为4组:(1)生理盐水对照组(Control);(2)褪黑素对照组(MT);(3)臭氧暴露组(2.14 mg·m-3 O3);(4)臭氧暴露+褪黑素保护组(2.14 mg·m-3 O3+MT)。最后一次臭氧暴露后,制备小鼠肺泡灌洗液,采用酶联免疫吸附法(ELISA)检测肺组织中IL-1β、IL-33、IL-4和IL-17A的含量;取部分肺组织制作肺匀浆并提取总mRNA,用于检测肺组织中丙二醛(MDA)和还原型谷胱甘肽(GSH)的含量,以及核因子E2相关因子2(Nrf2)、血红素加氧酶1(HO-1)、NADPH:醌氧化还原酶1(NQO-1)mRNA的表达。此外,采用苏木精-伊红染色(H&E stain)观察小鼠肺组织病理学改变。结果表明,与对照组相比,2.14 mg·m-3 O3暴露组小鼠肺组织MDA含量上升,IL-1β、IL-33、IL-4和IL-17A表达增加;GSH含量以及Nrf2HO-1NQO-1的mRNA相对表达量下降,且差异具有统计学意义(P<0.05或P<0.01)。与O3暴露组相比,MT保护组小鼠肺组织MDA含量下降,IL-1β、IL-33、IL-4和IL-17A表达下降,且GSH含量以及Nrf2HO-1NQO-1的mRNA相对表达量相应上升。此外,小鼠肺组织病理切片观察结果表明,O3暴露组小鼠肺组织出现炎细胞浸润和气道重塑现象,使用抗氧化剂MT处理后可减轻相应病理学改变。综上所述,2.14 mg·m-3 O3暴露可造成小鼠肺组织氧化损伤,诱发炎症,导致肺组织病理学改变;抗氧化剂的使用可增加Nrf2及其下游抗氧化酶的表达,缓解氧化应激,降低炎症因子水平,这验证了O3暴露引起的肺部损伤是通过氧化性损伤机制介导的。

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