生命早期PM2.5暴露对子代雄性大鼠前额皮层的影响*

doi:10.12047/j.cjap.6222.2022.001

中国应用生理学杂志 ›› 2022, Vol. 38 ›› Issue (1): 1-5.doi: 10.12047/j.cjap.6222.2022.001

• 研究论文 • 下一篇

生命早期PM_2.5暴露对子代雄性大鼠前额皮层的影响^*

梁晓天^1,2, 韩春蕾¹, 林本成², 石玥², 谢晓倩^1,2, 李康^2△, 袭著革^1,2△

1.滨州医学院公共卫生与管理学院, 山东烟台 264000;
2.军事科学院军事医学研究院环境医学与作业医学研究所, 天津 300050

收稿日期:2021-10-25 修回日期:2022-01-27 出版日期:2022-01-28 发布日期:2022-05-30
通讯作者: ^△Tel: 15222527225, 13682117760; E-mail: tjlikang@126.com, zhugexi2003@sina.com
基金资助:
* 国家自然科学基金面上项目(82073507);国家自然科学基金青年项目(81803270)

Effects of early life PM_2.5 exposure on prefrontal cortex of offspring male rats

LIANG Xiao-tian^1,2, HAN Chun-lei¹, LIN Ben-cheng², SHI Yue², XIE Xiao-qian^1,2, LI Kang^2△, XI Zhu-ge^1,2△

1. School of Public Health and Management, Binzhou Medical College, Yantai 264000;
2. Institute of Environmental Medicine and Occupational Medicine, Academy of Military Medicine, Academy of Military Sciences, Tianjin 300050, China

Received:2021-10-25 Revised:2022-01-27 Online:2022-01-28 Published:2022-05-30

摘要/Abstract

摘要： 目的: 探究生命早期不同阶段PM_2.5暴露对子代大鼠前额皮层的影响。方法: 将12只受孕后的SD孕鼠按体重随机分为对照组(CG)、母亲孕期暴露组(MG)、出生早期暴露组(EP)和全围产期暴露组(PP),每组3只。进行孕鼠与子鼠的清洁空气或8倍浓缩PM_2.5的暴露,其中CG组全程不暴露,MG组从妊娠第1日(GD1)暴露到GD21,EP组从出生第1日(PND1)暴露到PND21,PP组从GD1一直暴露到PND21。暴露完成后,取各组6只子代大鼠的前额皮层,采用HE染色进行病理学检测;酶联免疫吸附实验(ELISA)进行神经炎性因子检测;高效液相色谱-质谱分析进行神经递质检测;免疫印迹实验(Western blot)进行星形胶质细胞标志物检测;比色法进行脑组织氧化应激检测。结果: 与MG组和CG组子鼠比较,PP组和EP组子鼠前额皮层的病理学变化更加明显。与MG组和CG组子鼠比较,PP组和EP组大鼠的神经炎性因子IL-1、IL-6和TNF-α均显著增加(P＜0.01),且MT水平显著减少(P＜0.05),OT水平呈现下降趋势;神经递质Ach水平也显著增加(P＜0.01)。与MG组和CG组子鼠比较,PP组和EP组子鼠的GFAP水平呈升高趋势。与MG组和CG组子鼠比较,PP组和EP组子鼠的氧化应激指标SOD水平显著减少(P＜0.01),ROS水平显著增加(P＜0.01)。与CG组子鼠比较PP组子鼠的CAT水平显著减少(P＜ 0.01),与MG组子鼠比较PP组子鼠的CAT水平显著减少(P＜0.05);与CG组子鼠比较EP组子鼠的CAT水平显著减少(P＜0.05)。尚未发现PP组子鼠与EP组子鼠之间、MG组子鼠与CG组子鼠之间在IL-1、IL-6、TNF-α、MT、OT、Ach、GFAP、SOD、ROS和CAT水平存在差异。结论: 生命早期PM_2.5暴露可对子代雄性大鼠前额皮层产生不良影响,出生早期暴露可能更为敏感。

关键词: PM_2.5, 神经发育, 前额皮层, 敏感时期

Abstract: Objective: To investigate the effects of PM_2.5 exposure at different stages of early life on the prefrontal cortex of offspring rats. Methods: Twelve pregnant SD rats were randomly divided into four groups: Control group (CG), Maternal pregnancy exposure group (MG), Early postnatal exposure group (EP) and Perinatal period exposure group (PP), 3 rats in each group. The pregnant and offspring rats were exposed to clean air or 8-fold concentrated PM_2.5. MG was exposed from gestational day (GD) 1 to GD21. EP was exposed from postnatal day (PND) 1 to PND21, and PP was exposed from GD1 to PND21. After exposure, the prefrontal cortex of 6 offspring rats in each group was analyzed. HE staining was used to observe the pathological damage in the prefrontal cortex. ELISA was employed to detect neuroinflammatory factors, and HPLC/MSC was applied to determine neurotransmitter content. Western blot and colorimetry were applied for detecting astrocyte markers and oxidative stress markers, respectively. Results: Compared with MG and CG, the pathological changes of prefrontal cortex in PP and EP were more obvious. Compared with MG and CG, the neuroinflammatory factors (IL-1, IL-6, TNF-α) in PP and EP were increased significantly (P＜0.01), the level of MT were decreased significantly (P＜0.05), and the level of oxytocin (OT) showed a downward trend; the level of neurotransmitter ACh was also increased significantly (P＜0.01). Compared with MG and CG, the GFAP level of PP and EP showed an upward trend, the level of oxidative stress index SOD in PP and EP was decreased significantly (P＜0.01), and the level of ROS was increased significantly (P＜0.01). Compared with the offspring rats of CG and MG, the CAT level of PP was decreased significantly (P＜0.01, P＜0.05). Compared with the offspring rats of CG, the CAT level of EP was decreased significantly (P＜0.05). There was no significant difference in IL-1, IL-6, TNF-α, MT, OT, ACh, GFAP, SOD, ROS and CAT levels between PP and EP, or MG and CG. Conclusion: PM_2.5 exposure in early life has adverse effects on the prefrontal cortex of offspring male rats, and early birth exposure may be more sensitive.

Key words: PM_2.5, neurodevelopment, prefrontal cortex, sensitive period

中图分类号:

R122

梁晓天, 韩春蕾, 林本成, 石玥, 谢晓倩, 李康, 袭著革. 生命早期PM_2.5暴露对子代雄性大鼠前额皮层的影响^*[J]. 中国应用生理学杂志, 2022, 38(1): 1-5.

LIANG Xiao-tian, HAN Chun-lei, LIN Ben-cheng, SHI Yue, XIE Xiao-qian, LI Kang, XI Zhu-ge. Effects of early life PM_2.5 exposure on prefrontal cortex of offspring male rats[J]. CJAP, 2022, 38(1): 1-5.

参考文献

[1] Prüss-Ustün A, Wolf J, Corvalán C, et al. Preventing disease through healthy environments-a global assessment of the burden of disease from environmental risks[J]. Revue Dépidémiologie Et De Santé Publique, 2016, 64(5): 375.
[2] Liu Y, Zhang B, Zhang T, et al. Effect of NF-kappaB signal pathway on mucus secretion induced by atmospheric PM2.5 in asthmatic rats[J]. Ecotoxicol Environ Saf, 2020, 190: 110094.
[3] 田程远, 严明, 张云, 等. 杭州市中心城区大气PM2.5暴露致大鼠肺部损伤作用研究[J]. 中国应用生理学杂志, 2018, 34(4): 299-303.
[4] Lee B, Kim B, Lee K, Air pollution exposure and cardiovascular disease[J]. Toxicological Research, 2014, 30(2): 71-75.
[5] Association A P. The Diagnostic and Statistical Manual of Mental Disorders (DSM-V) [M]. Washington, DC: American Psychiatric Association, 2013.
[6] 方振, 胡西厚, 李康, 等. PM_(2.5)鼻腔滴注致小鼠海马组织损伤的炎性机制[J]. 中国应用生理学杂志, 2020, 36(3): 240-244.
[7] Zhang T, Zheng X, Wang X, et al. Maternal exposure to PM2.5 during pregnancy induces impaired development of cerebral cortex in mice offspring[J]. Int J Mol Sci, 2018, 19(1): 257.
[8] Liu J, Yang C, Yang J, et al. Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats[J]. Brain Behav, 2019, 9(12): e01453.
[9] McGuinn LA, Windham GC, Kalkbrenner AE, et al. Early life exposure to air pollution and autism spectrum disorder: Findings from a multisite case-control study[J]. Epidemiology, 2020, 31(1): 103-114.
[10] Rice D, Barone S. Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models[J]. Environmental Health Perspectives, 2000: 511-533.
[11] Fagundes LS, Fleck Ada S, Zanchi AC, et al. Direct contact with particulate matter increases oxidative stress in different brain structures[J]. Inhal Toxicol, 2015, 27(10): 462-467.
[12] Nephew BC, Nemeth A, Hudda N, et al. Traffic-related particulate matter affects behavior, inflammation, and neural integrity in a developmental rodent model[J]. Environ Res, 2020, 183: 109242.
[13] Heusinkveld HJ, Wahle T, Campbell A, et al. Neurodegenerative and neurological disorders by small inhaled particles[J]. Neurotoxicology, 2016, 56: 94-106.
[14] Yang CJ, Liu CL, Sang B, et al, The combined role of serotonin and interleukin-6 as biomarker for autism[J]. Neuroscience, 2015, 284: 290-296.
[15] Yang CJ, Tan HP, Yang FY, et al. The roles of cortisol and pro-inflammatory cytokines in assisting the diagnosis of autism spectrum disorder[J]. Res Autism Spectr Disord, 2015, 9: 174-181.
[16] Cohly HHP, Panja A. Immunological findings in autism[J]. Int Rev Neurobiol, 2005, 71: 317-341.
[17] Zhang S, Wu M, Peng C, et al. GFAP expression in injured astrocytes in rats[J]. Exp Ther Med, 2017, 14(3): 1905-1908.
[18] Klocke C, Allen JL, Sobolewski M, et al. Neuropathological consequences of gestational exposure to concentrated ambient fine and ultrafine particles in the mouse[J]. Toxicol Sci, 2017, 156(2): 492-508.
[19] Kulas JA, Hettwer JV, Sohrabi M, et al. In utero exposure to fine particulate matter results in an altered neuroimmune phenotype in adult mice[J]. Environ Pollut, 2018, 241: 279-288.
[20] Striepens N, Kendrick KM, Maier W, et al. Prosocial effects of oxytocin and clinical evidence for its therapeutic potential [J]. Front Neuroendocrinol, 2011, 32(4): 426-450.
[21] Averbeck BB, Bobin T, Evans S, et al. Emotion recognition and oxytocin in patients with schizophrenia[J]. Psychol Med, 2012, 42(2): 259-266.
[22] Zhang HF, Dai YC, Wu J, et al. Plasma oxytocin and arginine-vasopressin levels in children with autism spectrum disorder in China: Associations with symptoms[J]. Neurosci Bull, 2016, 32(5): 423-432.
[23] Guxens M, Lubczynska MJ, Muetzel RL, et al. Air pollution exposure during fetal life, brain morphology, and cognitive function in school-age children[J]. Biol Psychiatry, 2018, 84(4): 295-303.
[24] Wei H, Feng Y, Liang F, et al. Role of oxidative stress and DNA hydroxymethylation in the neurotoxicity of fine particulate matter[J]. Toxicology, 2017, 380: 94-103.

生命早期PM_2.5暴露对子代雄性大鼠前额皮层的影响^*

Effects of early life PM_2.5 exposure on prefrontal cortex of offspring male rats

PDF (PC)

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 3

编辑推荐

Metrics

本文评价

[1]	王亚洁, 袁博, 刘伟, 李玉皓, 苑晓勇. 纳米卟啉金属有机骨架对斑马鱼神经系统发育的作用^*[J]. 中国应用生理学杂志, 2020, 36(6): 662-667.
[2]	方振, 胡西厚, 李康, 韩洁, 田蕾, 闫峻, 张伟, 来文庆, 林本成, 刘晓华, 袭著革. PM_2.5鼻腔滴注致小鼠海马组织损伤的炎性机制[J]. 中国应用生理学杂志, 2020, 36(3): 240-244.
[3]	刘江涛, 罗斌, 贺小桃, 李兰玉, 徐生刚. 维生素E对暴露于高温及PM_2.5中COPD大鼠呼吸系统的保护性作用^*[J]. 中国应用生理学杂志, 2019, 35(4): 293-296.

生命早期PM2.5暴露对子代雄性大鼠前额皮层的影响*

Effects of early life PM2.5 exposure on prefrontal cortex of offspring male rats

PDF (PC)

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 3

编辑推荐

Metrics

本文评价

生命早期PM_2.5暴露对子代雄性大鼠前额皮层的影响^*

Effects of early life PM_2.5 exposure on prefrontal cortex of offspring male rats