Secondary brain injury after polystyrene microplastic-induced intracerebral hemorrhage is associated with inflammation and pyroptosis
Unlike regular environmental pollutants, microplastics cannot dissolve in liquids. Physical contact of microplastic (MPs) with tissue can damage tissue structure, and it is unclear how this physical secondary injury affects brain tissue. Through CTD database analysis, it was determined that cerebral...
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Veröffentlicht in: | Chemico-biological interactions 2022-11, Vol.367, p.110180-110180, Article 110180 |
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Sprache: | eng |
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Zusammenfassung: | Unlike regular environmental pollutants, microplastics cannot dissolve in liquids. Physical contact of microplastic (MPs) with tissue can damage tissue structure, and it is unclear how this physical secondary injury affects brain tissue. Through CTD database analysis, it was determined that cerebral ischemia may be one of the main ways of brain tissue damage caused by MPs, and inflammatory response may play a key role in it. In the present study, PS-MPs (L-PS group:1 mg/L, M − PS group:10 mg/L, H-PS group: 100 mg/L in water) were assessed to brain tissue damage in chicken after six weeks of continuous exposure. Exposure to PS-MPs caused cerebral hemorrhage as well as generation of microthrombi and loss of Purkinje cells. Intracerebral hemorrhage caused a strong infiltration of inflammatory cells and activated the ASC-NLRP3-GSDMD signaling pathway to induce pyroptosis. Disruption of mitochondrial dynamics by PS-MPs exposure disrupts mitochondrial function and activates AMPK signaling. In conclusion, this study explored the mechanism regulation of subsequent brain injury from the perspective of physical injury (cerebral hemorrhage) of PS-MPs. To provide a reference for elucidating the neurotoxicity induced by microplastic exposure.
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•Exposure to PS-MPs caused hemorrhage in chicken brain tissue.•PS-MPs disrupt mitochondrial dynamic homeostasis, leading to dysfunction.•In response to mitochondrial damage, the AMPK signaling pathway is activated. |
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ISSN: | 0009-2797 1872-7786 |
DOI: | 10.1016/j.cbi.2022.110180 |