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Effects of atmospheric PM2.5 subchronic exposure on fibrosis, inflammation, endoplasmic reticulum stress and apoptosis in livers of rats

Abstract

Epidemiological studies revealPM2.5 exposure islinked to liver cancer. However, the hepatic toxicity and relevant molecularmechanisms of PM2.5 have not yet been fully described.Here we sought to investigate the fibrosis, inflammation, endoplasmicreticulum (ER) stress and apoptosisin livers of rats caused by PM2.5during summer and winter in Taiyuan of China. Male SD rats were subchronically exposed to PM2.5 (for summer: 0.2, 0.6, 1.5 mg/kgb.w.; for winter: 0.3, 1.5, 2.7 mg/kg b.w.) via intratracheal instillation once every 3 days for 60 days. The results showed that high dosage PM2.5 (1) caused hepatic histopathological changes and liver function decline though elevating activities of AST, ALT, CYP450 and GST; (2) triggered liver fibrosis, in which TGF-β, Col Ⅰ, Col Ⅲ, and MMP13 mRNA and protein expression were significantly upregulated, and enhanced inflammation with the overexpression of TNF-α, IL-6 and HO-1 versus the control; (3) induced liver ER stress and cell apoptosis via activating the GRP78/ATF6/CHOP/TRB3/caspase12 pathway. The data also indicated that the liver injury induced by winter PM2.5 of Taiyuan was more serious than summer PM2.5. This work will provide new insight into the mechanisms of PM2.5-induced liver injury, and be informative to understand the underlying mechanisms by which PM2.5 might affect liver diseases.

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Publication details

The article was received on 02 Oct 2017, accepted on 02 Jan 2018 and first published on 10 Jan 2018


Article type: Paper
DOI: 10.1039/C7TX00262A
Citation: Toxicol. Res., 2018, Accepted Manuscript
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    Effects of atmospheric PM2.5 subchronic exposure on fibrosis, inflammation, endoplasmic reticulum stress and apoptosis in livers of rats

    R. Li, M. Zhang, Y. Wang, K. K. Yung, R. Su, Z. Li, L. Zhao, C. Dong and Z. Cai, Toxicol. Res., 2018, Accepted Manuscript , DOI: 10.1039/C7TX00262A

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