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微塑料暴露通过诱导 ROS 信号导致人肺上皮细胞和小鼠肺部衰老。

Microplastics exposure causes the senescence of human lung epithelial cells and mouse lungs by inducing ROS signaling.

机构信息

Beijing Advanced Innovation Center for Food Nutrition and Human Health, Department of Nutrition and Health, China Agricultural University, Beijing 100193, China.

College of Food Science and Engineering, Gansu Agricultural University, Lanzhou 730070, China.

出版信息

Environ Int. 2024 Mar;185:108489. doi: 10.1016/j.envint.2024.108489. Epub 2024 Feb 8.

Abstract

Microplastics (MPs) are environmental pollutants and can be inhaled by humans to threaten health. The lung tissue, responsible for the gas exchange between the body and the environment, is vulnerable to MPs exposure. However, from the perspective of cellular senescence, the effect of MPs on lung cells and tissues has not yet been deeply dissected. In this study, we reported that all the four typical MPs exhibited the significant biological effects in term of inducing senescence of human lung derived cells A549 and BEAS-2B in vitro. We further found that polyvinyl chloride (PVC) increased the reactive oxygen species (ROS) level in A549 cells and that PVC-induced senescent characteristics could be largely reversed by antioxidant treatment. Importantly, intratracheal instillation of PVC MPs in mice could effectively impair their physical function, induce the increased systemic inflammation level, cause the accumulation of senescent cells. Our study demonstrates that MPs induce senescence in human lung epithelial cells and mouse lungs by activating ROS signaling, and provides new insight into the potential pathogenesis of MPs on lung diseases.

摘要

微塑料(MPs)是环境污染物,可被人类吸入从而威胁健康。肺部组织负责人体与环境之间的气体交换,易受到 MPs 暴露的影响。然而,从细胞衰老的角度来看, MPs 对肺细胞和组织的影响尚未被深入剖析。在这项研究中,我们报道了所有四种典型的 MPs 在体外均能显著诱导人肺源细胞 A549 和 BEAS-2B 衰老。我们进一步发现聚氯乙烯(PVC)增加了 A549 细胞中的活性氧(ROS)水平,而抗氧化剂处理可显著逆转 PVC 诱导的衰老特征。重要的是,气管内滴注 PVC MPs 可有效损害小鼠的体力活动,引起全身性炎症水平升高,并导致衰老细胞的积累。我们的研究表明 MPs 通过激活 ROS 信号诱导人肺上皮细胞和小鼠肺部衰老,并为 MPs 对肺部疾病的潜在发病机制提供了新的见解。

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