活性氧（ROS）拮抗 Parkin 介导的线粒体自噬对铝诱导的小鼠肝脏炎症损伤的保护作用。
ROS antagonizes the protection of Parkin-mediated mitophagy against aluminum-induced liver inflammatory injury in mice.
机构信息
Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
出版信息
Food Chem Toxicol. 2022 Jul;165:113126. doi: 10.1016/j.fct.2022.113126. Epub 2022 May 12.
Aluminum (Al) is a food pollutant that has extensive deleterious effects on the liver. Our previous research proposed that E3 ubiquitin ligase PARK2 knockout (Parkin) could aggravate Al-induced liver damage by inhibiting mitophagy, during which the reactive oxygen species (ROS) content increases. Inhibition of mitophagy can activate inflammasome. But the link between Parkin-mediated mitophagy and liver inflammatory injury caused by Al, and the role of ROS in it remain unclear. In this study, we applied Al, Parkin and N-acetyl-L-cysteine (NAC) to act on C57BL/6N mice to investigate them. We found that Al could induce liver inflammatory injury and Parkin could aggravate it. Meanwhile, inhibition of ROS alleviated oxidative stress, mitochondrial damage, mitophagy and inflammatory injury caused by Al in Parkin mice liver. These results indicated that ROS antagonized the protection of Parkin-mediated mitophagy against Al-induced liver inflammatory damage in mice.
铝（Al）是一种食物污染物，对肝脏有广泛的有害影响。我们之前的研究提出，E3 泛素连接酶 PARK2 敲除（Parkin）可以通过抑制线粒体自噬来加重铝诱导的肝损伤，在此过程中，活性氧（ROS）含量增加。线粒体自噬的抑制可以激活炎性体。但是 Parkin 介导的线粒体自噬与铝引起的肝炎症性损伤之间的联系，以及 ROS 在其中的作用尚不清楚。在这项研究中，我们应用铝、Parkin 和 N-乙酰-L-半胱氨酸（NAC）作用于 C57BL/6N 小鼠进行研究。我们发现铝可以诱导肝炎症性损伤，而 Parkin 可以加重这种损伤。同时，抑制 ROS 可以减轻 Parkin 敲除小鼠肝脏中铝引起的氧化应激、线粒体损伤、线粒体自噬和炎症性损伤。这些结果表明，ROS 拮抗了 Parkin 介导的线粒体自噬对铝诱导的小鼠肝炎症性损伤的保护作用。
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