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Lias overexpression alleviates pulmonary injury induced by fine particulate matter in mice

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Abstract

Oxidative stress and inflammation are mechanisms underlying toxicity induced by fine particulate matter (PM2.5). The antioxidant baseline of the human body modulates the intensity of oxidative stress in vivo. This present study aimed to evaluate the role of endogenous antioxidants in alleviating PM2.5-induced pulmonary injury using a novel mouse model (LiasH/H) with an endogenous antioxidant capacity of approximately 150% of its wild-type counterpart (Lias+/+). LiasH/H and wild-type (Lias+/+) mice were randomly divided into control and PM2.5 exposure groups (n = 10), respectively. Mice in the PM2.5 group and the control group were intratracheally instilled with PM2.5 suspension and saline, respectively, once a day for 7 consecutive days. The metal content, major pathological changes in the lung, and levels of oxidative stress and inflammation biomarkers were examined. The results showed that PM2.5 exposure induced oxidative stress in mice. Overexpression of the Lias gene significantly increased the antioxidant levels and decreased inflammatory responses induced by PM2.5. Further study found that LiasH/H mice exerted their antioxidant function by activating the ROS-p38MAPK-Nrf2 pathway. Therefore, the novel mouse model is useful for the elucidation of the mechanisms of pulmonary injury induced by PM2.5.

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Abbreviations

BALF:

Bronchoalveolar lavage fluid

COPD:

Chronic obstructive pulmonary disease

CAT:

Catalase

GSH:

Reduced glutathione

GCLC:

Glutamate-cysteine ligase

HO-1:

Haemoxygenase-1

NQO1:

NAD(P)H quinone oxidoreductase 1

KEAP1:

Kelch-like ECH-associated protein-1

LA:

α-Lipoic acid

Lias:

Lipoic acid synthase

MAPK:

Mitogen-activated protein kinase

MDA:

Malondialdehyde

MCP-1:

Monocyte chemoattractant protein-1

Nrf2:

Nuclear factor erythroid 2-related factor 2

SOD2:

Superoxide dismutase 2

ROS:

Reactive oxygen species

TAC:

Total antioxidation capacity

TNF-α :

Tumor necrosis factor-α

IL-1β :

Interleukin-1β

IL-6:

Interleukin-6

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Acknowledgements

We appreciate the support of the Nature Science Foundation of Henan Provincial (222300420516), the National Natural Science Foundation of China (81703183, 81773399, 81573112), the International Cooperation and Exchange Project of NSFC (81961128031) and the Scientific and Technological Research Project of Henan Provincial (222102320325 and 212102310643).

Funding

This work was supported by grant 222300420516, 81703183, 81773399, 81573112, 81961128031, 222102320325 and 212102310643. Guangcui Xu has received research support from the Nature Science Foundation of Henan Provincial and the National Natural Science Foundation of China. Weidong Wu has received research support from the National Natural Science Foundation of China and International cooperation and exchange project of NSFC. Qiyu Gao and Zhen An have received research support from the Scientific and Technological Research Project of Henan Provincial.

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  1. School of Public Health, Xinxiang Medical University, Xinxiang, 453003, Henan, People’s Republic of China

    Guangcui Xu, Yingzheng Zhao, Yingjun Tao, Cheng Xiong, Mengdi Lv, Qiyu Gao, Fengquan Zhang, Zhen An & Weidong Wu

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  1. Guangcui Xu
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Contributions

GX and WW designed this project and writing draft. GX, YT, CX, QG completed the experimental work. YZ, ZA performed software work and data curation. ML and FZ did animal housework.

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Correspondence to Weidong Wu.

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Animal care and use were in following the guidelines of the Animal Ethics Committee from Xinxiang Medical University (No. XYLL-2017086).

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Xu, G., Zhao, Y., Tao, Y. et al. Lias overexpression alleviates pulmonary injury induced by fine particulate matter in mice. Environ Geochem Health 45, 6585–6603 (2023). https://doi.org/10.1007/s10653-023-01651-3

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