PPARγ/UCP2在甲醛致学习记忆障碍中的作用

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摘要为探究过氧化物酶体增殖物激活受体γ/解偶联蛋白2（PPARγ/UCP2）在甲醛（FA）诱导的学习记忆障碍中的作用，本文将C57BL/6小鼠随机分为：对照组、T0070907组（抑制剂组）、3mg/m³ FA组、3mg/m³ FA+T0070907组，进行连续21d的实验暴露，在第22d取脑组织测定脑组织脏体比并匀浆，检测活性氧（ROS）、谷胱甘肽（GSH）、丙二醛（MDA）、核因子κB （NF-κB）、白细胞介素6（IL-6）、PPARγ、UCP2等生化指标，通过Nissl染色观察脑组织的病理学变化.结果发现，与对照组相比，T0070907组和3mg/m³ FA组小鼠大脑皮层神经元受损，GSH含量下降，ROS、MDA、NF-κB、IL-6含量有所上升，而3mg/m³ FA+T0070907组小鼠上述现象更严重.此外，与对照组相比，T0070907组小鼠脑组织中的PPARγ和UCP2含量下降，但3mg/m³ FA组小鼠脑组织中的PPARγ和UCP2含量上升；与3mg/m³ FA组相比，加入抑制剂的3mg/m³ FA+T0070907组小鼠脑组织中的PPARγ和UCP2含量下降.研究结果表明，在加入PPARγ抑制剂后，PPARγ/UCP2含量下降，加重了FA所致小鼠的学习记忆障碍，故PPARγ/UCP2在FA致学习记忆障碍中可能起保护作用.

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	郑丽芳
	萧嘉莉
	袁佩昕
	陈泊岐
	梅琼
	池煜瑶
	吕柯
	李睿

关键词 ：甲醛, 记忆功能, 氧化损伤, 炎症

Abstract：To investigate the possible role of peroxisome proliferators-activated receptor γ/uncoupling protein 2(PPARγ/UCP2) in learning and memory impairment induced by formaldehyde(FA), C57BL/6 mice were randomly divided into different groups including control group, T0070907group(inhibitor group), 3mg/m³ FA group, 3mg/m³ FA+T0070907 group. After 21 days of continuous exposure to FA or other treatments in the experiment, mouse brain tissue was taken to determine brain index and before being homogenized for the detection of a series of physiological indices such as reactive oxygen species(ROS), glutathione(GSH), malondialdehyde(MDA), nuclear factor κB(NF-κB), interleukin-6(IL-6), PPARγ, UCP-2, as well as the determination of pathological changes by observing the Nissl stained brain tissue. The results showed that compared with those of mice in the control group, the cerebral cortex neurons of the mice were damaged in the T0070907group and the 3mg/m³ FA group, the content of GSH decreased, and the levels of ROS, MDA, NF-κB, and IL-6 increased, with even more severe results were found in mice from the 3mg/m³ FA+T0070907 group. In addition, compared with the control group, the contents of PPARγ and UCP2 decreased in the brain tissue of mice in the T0070907 group, while increased in those from the 3mg/m³ FA group; compared with those of mice from the 3mg/m³ FA group, the contents of PPARγ and UCP2 decreased in the brain tissue of mice from the 3mg/m³ FA+T0070907 group after the inhibitor was administered. The content of PPARγ/UCP2 decreased after addition of T0070907, the inhibitor of PPARγ, which aggravated the learning and memory impairment in mice induced by FA exposure, therefore PPARγ/UCP2 may be protective to mice from the learning and memory impairment induced by FA.

Key words： formaldehyde learning and memory oxidative damage inflammation

收稿日期: 2020-11-19

PACS:

X18

基金资助:国家自然科学基因项目（21103059）；科技部十三五国家重点研发计划项目（2017YFC0702700）

通讯作者: 李睿,教授,ruli@mail.ccnu.edu.cn E-mail: ruli@mail.ccnu.edu.cn

作者简介: 郑丽芳(1996-),女,山西应县人,华中师范大学硕士研究生,研究方向为环境分子生物医学.发表论文1篇.

引用本文:

郑丽芳, 萧嘉莉, 袁佩昕, 陈泊岐, 梅琼, 池煜瑶, 吕柯, 李睿. PPARγ/UCP2在甲醛致学习记忆障碍中的作用[J]. 中国环境科学, 2021, 41(6): 2923-2931. ZHENG Li-fang, XIAO Jia-li, YUAN Pei-xin, CHEN Bo-qi, MEI Qiong, CHI Yu-yao, LV Ke, LI Rui. Role of the PPARγ/UCP2 in learning and memory impairment induced by formaldehyde. CHINA ENVIRONMENTAL SCIENCECE, 2021, 41(6): 2923-2931.

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http://www.zghjkx.com.cn/CN/ 或 http://www.zghjkx.com.cn/CN/Y2021/V41/I6/2923

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