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PS-MPs Induced Inflammation and Phosphorylation of Inflammatory Signalling Pathways in Liver

Toxics 2024 1 citation ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Mengchao Ying, Naimin Shao, Cheng Dong, Yijie Sha, Chen Li, Xinyu Hong, Yu Ding, Jing Xu, Kelei Qian, Gonghua Tao, Ping Xiao

Summary

Polystyrene microplastics (0.1 µm) induced inflammatory responses and activated multiple inflammatory signalling pathways in mouse and human liver cell lines after 28 days of exposure. The study identified specific phosphorylation cascades through which PS MPs trigger hepatic inflammation, linking microplastic exposure to liver damage mechanisms.

Polymers
Body Systems
Models

As new pollutants, microplastics (MPs) have attracted much attention worldwide because they cause serious environmental pollution and pose potential health risks to humans. However, the toxic effects of MPs are still unclear. In this study, we analysed the inflammatory effects of 0.1 μm polystyrene microplastics (PS-MPs) on mouse and human liver cell lines. After 28 days of exposure to PS-MPs, the mice presented decreased liver index values and increased AST/ALT values. HL7702 and HepG2 were treated with PS-MPs for 24 h, and the cytotoxicity, the expression levels of inflammatory factors, and the phosphorylation of proteins in inflammation related pathways were confirmed. Compared with the control, the cell viability of these two cells significantly decreased after exposure to the PS-MPs at 1000 μm/cm2, and the BMD model also exhibited a similar dose. LDH leakage and AST also increased in a dose-dependent increase after PS-MPs exposure. The relative levels of chemokines such as GM-CSF, IL-6, IL-8, and IL-12p70 were significantly greater than those in the control. Furthermore, the PS-MPs can increase the expression levels of TLR4, MyD88, and NF-κB and activate the phosphorylation of NF-κB and STATs. Based on these results, exposure to PS-MPs can stimulate liver inflammation and activate the TLR4/MyD88/NF-κB and JAK-STAT pathways.

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