College of Medical Laboratory, Dalian Medical University, Dalian, Liaoning Province, China.
Environmental Monitoring Station of Langfang, Langfang Environmental Protection Bureau, Langfang, Hebei Province, China.
Environ Toxicol. 2021 Sep;36(9):1765-1774. doi: 10.1002/tox.23297. Epub 2021 May 26.
Fine particulate matter (PM ) 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 . However, the effect of PM 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 in the brain and BV2 microglial cells. PM 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 PM exposure increased the level of autophagy. After exposure to PM , the levels of 5'-adenosine monophosphate-activated protein kinase (AMPK) increased, while the levels of mammalian target of rapamycin (mTOR) decreased, suggesting that PM might induce autophagy by activating the AMPK/mTOR pathway. In addition, CEOs alleviated oxidative stress and autophagy induced by PM . Therefore, we concluded that CEOs reduce oxidative stress induced by PM exposure by inhibiting autophagy via the AMPK/mTOR signaling pathway, and these findings provide new opportunities for the prevention of PM -induced brain diseases.
细颗粒物 (PM ) 可能会损害呼吸系统并导致呼吸道疾病。已证实复合精油 (CEOs) 可减轻 PM 对肺部和巨噬细胞的损伤。然而,PM 暴露对大脑的影响很少被研究。当大脑发生氧化应激时,它很容易引起神经疾病。自噬密切参与许多生理过程,尤其是对大脑很重要的过程。自噬受阻或过度会导致一系列脑部疾病,如脑缺血和中风。本研究调查了 CEOs 是否调节过度自噬并减轻 PM 在大脑和 BV2 小胶质细胞中引起的氧化应激。PM 增加了 ROS、Nox2、NF-κB 和 MDA 的水平,同时降低了超氧化物歧化酶和 HO-1 的水平,导致大脑发生氧化应激。LC3 水平升高和 P62 水平降低表明 PM 暴露增加了自噬水平。PM 暴露后,5'-腺嘌呤单磷酸激活蛋白激酶 (AMPK) 的水平增加,而雷帕霉素靶蛋白 (mTOR) 的水平降低,表明 PM 可能通过激活 AMPK/mTOR 通路诱导自噬。此外,CEOs 减轻了 PM 引起的氧化应激和自噬。因此,我们得出结论,CEOs 通过抑制 AMPK/mTOR 信号通路减少 PM 暴露引起的氧化应激和自噬,这些发现为预防 PM 引起的脑部疾病提供了新的机会。