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

Area of Science:

• Environmental Science
• Toxicology
• Cell Biology

Background:

• Microplastics (MPs) are emerging pollutants with widespread environmental presence.
• The toxicological effects of MPs, particularly on human health, remain incompletely understood.
• Liver exposure to MPs is a growing concern due to potential health implications.

Purpose of the Study:

• To investigate the inflammatory effects of 0.1 μm polystyrene microplastics (PS-MPs) on mouse and human liver cell lines.
• To elucidate the molecular mechanisms underlying PS-MP-induced liver inflammation.
• To assess the impact of PS-MPs on liver function and cellular integrity.

Main Methods:

• Exposure of mice and liver cell lines (HL7702, HepG2) to varying concentrations of PS-MPs.
• Analysis of liver index, AST/ALT levels, and lactate dehydrogenase (LDH) leakage in mice.
• Assessment of cell viability, inflammatory factor expression (GM-CSF, IL-6, IL-8, IL-12p70), and protein phosphorylation (NF-κB, STATs) in vitro.
• Investigation of the Toll-like receptor 4 (TLR4)/MyD88/NF-κB and JAK-STAT signaling pathways.

Main Results:

• PS-MP exposure in mice led to decreased liver index and elevated AST/ALT values.
• In vitro, PS-MPs reduced liver cell viability and increased LDH leakage in a dose-dependent manner.
• Significant upregulation of inflammatory chemokines (GM-CSF, IL-6, IL-8, IL-12p70) was observed.
• PS-MPs activated the TLR4/MyD88/NF-κB and JAK-STAT signaling pathways, indicated by increased expression and phosphorylation of key proteins.

Conclusions:

• Exposure to polystyrene microplastics stimulates liver inflammation.
• PS-MPs activate the TLR4/MyD88/NF-κB and JAK-STAT signaling pathways in liver cells.
• These findings highlight the potential hepatotoxicity of microplastics and warrant further investigation into their health risks.