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中国精品科技期刊2020
刘旭东,张智淮,杨建邦,等. 增塑剂乙酰柠檬酸三丁酯暴露对学习记忆能力的影响及VE保护作用[J]. 食品工业科技,2021,42(12):233−240. doi: 10.13386/j.issn1002-0306.2020110300.
引用本文: 刘旭东,张智淮,杨建邦,等. 增塑剂乙酰柠檬酸三丁酯暴露对学习记忆能力的影响及VE保护作用[J]. 食品工业科技,2021,42(12):233−240. doi: 10.13386/j.issn1002-0306.2020110300.
LIU Xudong, ZHANG Zhihuai, YANG Jianbang, et al. Effects of Plasticizer Acetyl Tributyl Citrate Exposure on Learning and Memory Abilities and Protective Effects of Vitmain E [J]. Science and Technology of Food Industry, 2021, 42(12): 233−240. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2020110300.
Citation: LIU Xudong, ZHANG Zhihuai, YANG Jianbang, et al. Effects of Plasticizer Acetyl Tributyl Citrate Exposure on Learning and Memory Abilities and Protective Effects of Vitmain E [J]. Science and Technology of Food Industry, 2021, 42(12): 233−240. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2020110300.

增塑剂乙酰柠檬酸三丁酯暴露对学习记忆能力的影响及VE保护作用

Effects of Plasticizer Acetyl Tributyl Citrate Exposure on Learning and Memory Abilities and Protective Effects of Vitmain E

  • 摘要: 为探究增塑剂乙酰柠檬酸三丁酯(Acetyl Tributyl Citrate, ATBC)暴露对学习记忆能力的影响以及维生素E(Vitmain E,VE)的保护作用。采用灌胃暴露的方式对C57BL/6小鼠进行连续90 d的ATBC暴露(200 mg/kg·day),另设VE保护组,在ATBC暴露同时进行50 mg/kg·day VE灌胃。通过Morris水迷宫实验和跳台实验检测各组小鼠的学习记忆能力,观察小鼠脑组织损伤程度,检测小鼠脑组织氧化应激和炎症反应水平进行检测。结果显示,在该实验条件下ATBC暴露会导致小鼠学习记忆障碍;脑海马组织和大脑皮层结构异常;脑组织活性氧(reactive oxygen species,ROS)、丙二醛(malondialdehyde,MDA)、4-羟基壬烯酸(4-hydroxynoneal,4-HNE)含量显著性上升(P<0.05),而还原型谷胱甘肽(glutathione,GSH)含量及超氧化物歧化酶(superoxide dismutase,SOD)活性出现下降;小鼠脑组织核转录因子(Nuclear transcription,NF-κB)、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)、白介素1β(Interleukin-1β,IL-1β)水平显著上升(P<0.05)。而同时进行VE灌胃后,保护组小鼠学习记忆能力显著性提高(P<0.05),脑海马组织和大脑皮层结构异常有所改善,脑组织ROS、MDA、4-HNE、NF-κB、TNF-α、IL-1β含量显著性下降(P<0.05),GSH含量和SOD活性出现显著性上升(P<0.05)。本研究说明200 mg/kg·day ATBC连续90 d的灌胃暴露会引起小鼠学习记忆障碍和脑组织损伤,而VE可以通过下调脑组氧化应激和炎症水平对小鼠脑组织进行保护,学习记忆障碍有显著改善。

     

    Abstract: In order to investigate the effects of plasticizer acetyl tributyl citrate (ATBC) exposure on learning and memory abilities and protective effects of vitmain E (VE). C57BL/6 mice were exposed to 200 mg/kg·day for 90 days by gavage, and the VE gavage was performed at 50 mg/kg·day during ATBC exposure as a VE protection group. The learning and memory abilities were detected by Morris water maze test and Step-down passive avoidance test, the pathological changes of brain tissue were observed, the oxidative stress and inflammation levels in mice brain were detected. Results showed that under the experimental conditions, ATBC exposure induced learning and memory disorder, abnormal structure of hippocampus and cerebral cortex in mice; the content of reactive oxygen species (ROS), malondialdehyde (MDA) and 4-hydroxynoneal (4-HNE) in mice brain increased, while glutathione (GSH) content and activity of superoxide dismutase (SOD) decreased, and the expression of nuclear transcription κB (NF-κB), tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) increased. After VE gavage, the learning and memory disorder of the mice in the protection group was significantly recovered (P<0.05), hippocampus and cerebral cortex tissue abnormalities were improved, the contents of ROS, MDA, 4-HNE, NF-κB, TNF-α and IL-1β in the brain tissues significantly decreased (P<0.05), and the GSH contents and SOD activity significantly increased (P<0.05). This study showed that gavage exposure of 200 mg/kg·day ATBC for 90 days could induce learning and memory disorder and brain damage in mice, while VE could protect the brain tissue of mice by reducing the levels of oxidative stress and inflammation, and the learning and memory abilities were significantly improved.

     

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