首页> 外文期刊>Environmental toxicology >Compound essential oils relieve oxidative stress caused by PM_(2.5) exposure by inhibiting autophagy through the AMPK/ mTOR pathway
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Compound essential oils relieve oxidative stress caused by PM_(2.5) exposure by inhibiting autophagy through the AMPK/ mTOR pathway

机译:复合精油通过AMPK / MTOR途径抑制自噬抑制自噬引起的PM_(2.5)暴露引起的氧化应激

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摘要

Fine participate matter (PM_(2.5)) potentially damages the respiratory system and causes respiratory diseases. Compound essential oils (CEOs) have been shown to alleviate the damage to the lung and macrophages caused by PM_(2.5). However, the effect of PM_(2.5) exposure on the brain has rarely been investigated. When oxidative stress occurs in the brain, it readily causes neurological diseases. Autophagy is intimately involved in many physiological processes, especially processes important for the brain. Blocked or excessive autophagy causes a series of brain diseases, such as cerebral ischemia and stroke. This study investigated whether CEOs regulate excessive autophagy and reduce the oxidative stress caused by PM_(2.5) in the brain and BV2 microglial cells. PM_(2.5) increased the levels of ROS, Nox2, NF-κB and MDA while decreasing superoxide dismutase and HO-1 levels, which led to oxidative stress in the brain. The increased LC3 level and decreased P62 level suggested that PM2.5 exposure increased the level of autophagy. After exposure to PM_(2.5), the levels of 5'-adenosine monophosphate-activated protein kinase (AMPK) increased, while the levels of mammalian target of rapamycin (mTOR) decreased, suggesting that PM2.5 might induce autophagy by activating the AMPK/mTOR pathway. In addition, CEOs alleviated oxidative stress and autophagy induced by PM_(2.5). Therefore, we concluded that CEOs reduce oxidative stress induced by PM_(2.5) exposure by inhibiting autophagy via the AMPK/mTOR signaling pathway, and these findings provide new opportunities for the prevention of PM_(2.5)-induced brain diseases.
机译:精细参与物(PM_(2.5))可能会损害呼吸系统并导致呼吸系统疾病。已显示复合精油(CEOS)以缓解由PM_(2.5)引起的肺和巨噬细胞的损伤。然而,PM_(2.5)暴露在大脑上的影响很少被调查。当氧化应激发生在大脑中时,它容易导致神经疾病。自噬涉及许多生理过程,特别是对大脑重要的过程。阻塞或过量的自噬导致一系列脑病,例如脑缺血和中风。本研究研究了CEO是否调节过量的自噬并降低脑和BV2小胶质细胞中PM_(2.5)引起的氧化应激。 PM_(2.5)增加ROS,NOX2,NF-κB和MDA的水平,同时降低超氧化物歧化酶和HO-1水平,导致大脑中的氧化应激。 LC3水平增加和P62水平降低表明PM2.5暴露增加了自噬的水平。暴露于PM_(2.5)后,5'-腺苷活化蛋白激酶(AMPK)的水平增加,而雷帕霉素(MTOR)的哺乳动物靶标的水平降低,表明PM2.5可能通过激活安培诱导自噬。 / mtor途径。此外,CEO缓解了PM_(2.5)诱导的氧化应激和自噬。因此,我们得出结论,CEO通过通过AMPK / MTOR信号通路抑制自噬降低PM_(2.5)曝光的氧化应激,这些发现为预防PM_(2.5)诱导的脑病提供了新的机会。

著录项

  • 来源
    《Environmental toxicology》 |2021年第10期|1765-1774|共10页
  • 作者单位

    College of Medical Laboratory Dalian Medical University Dalian Liaoning Province China;

    College of Medical Laboratory Dalian Medical University Dalian Liaoning Province China;

    College of Medical Laboratory Dalian Medical University Dalian Liaoning Province China;

    College of Medical Laboratory Dalian Medical University Dalian Liaoning Province China;

    College of Medical Laboratory Dalian Medical University Dalian Liaoning Province China;

    Environmental Monitoring Station of Langfang Langfang Environmental Protection Bureau Langfang Hebei Province China;

    College of Medical Laboratory Dalian Medical University Dalian Liaoning Province China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    AMPK/mTOR pathway; autophagy; compound essential oils; oxidative stress; PM_(2.5);

    机译:AMPK / MTOR途径;自噬;复合精油;氧化胁迫;PM_(2.5);

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