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Cerebral neurotoxicity of amino-modified polystyrene nanoplastics in mice and the protective effects of functional food Camellia pollen

The Science of The Total Environment 2023 31 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.

Yanliang Wu, Yining Zhu, Yanliang Wu, Hangjia Bai, Yanliang Wu, Yanliang Wu, Yanliang Wu, Yanliang Wu, Hangjia Bai, Fenghe Wang Yanliang Wu, Ruijie Che, Yanliang Wu, Fenghe Wang, Ruijie Che, Fenghe Wang, Haini Li, Ruijie Che, Haini Li, Fenghe Wang Hangjia Bai, Hangjia Bai, Fenghe Wang Hangjia Bai, Ruijie Che, Fenghe Wang, Fenghe Wang, Yining Zhu, Hangjia Bai, Ruijie Che, Fenghe Wang Ruijie Che, Ruijie Che, Fenghe Wang, Fenghe Wang, Chaofeng Zhang, Fenghe Wang, Fenghe Wang, Fenghe Wang Fenghe Wang Fenghe Wang, Fenghe Wang Fenghe Wang Chaofeng Zhang, Chaofeng Zhang, Fenghe Wang Fenghe Wang Fenghe Wang, Fenghe Wang, Fenghe Wang, Fenghe Wang

Summary

In a mouse study, amino-modified polystyrene nanoplastics crossed the blood-brain barrier and accumulated in brain tissue, activating genes associated with Alzheimer's disease. The nanoplastics damaged the protective barrier around the brain, triggered harmful processes in neurons, and promoted the formation of a protein linked to brain degeneration. The research also found that Camellia pollen, a natural food product, could partially protect the brain from this nanoplastic-induced damage.

Polymers

Body Systems

Nervous

Models

Mouse

Study Type In vitro

Accumulating evidence suggests that nanoplastics contribute to an increased risk of brain damage, however, the precise underlying mechanisms remain unclear. Here, we subjected mice to long-term exposure to amino-modified polystyrene nanoplastics (APS-NPs). These nanoplastics were detected in the mouse brain; coupled with the observed upregulation of Alzheimer's disease-associated genes (APP and MAPT). To further explore nanoplastic damage mechanisms and the corresponding protective strategies against these mechanisms in vitro, we used hCMEC/D3 and HT22 cells. Results showed that APS-NPs disrupted tight junction proteins (Occludin and ZO-1) via TLR2/MMP9 axis, resulting in blood-brain barrier permeation; this was significantly mitigated by functional food Camellia pollen treatment. APS-NPs initiated iNOS and nNOS upregulation within neurons resulting in Sirtuin 1 deacetylase inactivation and CBP acetyltransferase stimulation, ultimately leading to Ac-Tau formation. This process was attenuated by Camellia pollen, which also ameliorated the APS-NPs-induced neuronal apoptosis mediated by the p53/Bax/Bcl-2 axis. Network pharmacology analysis of Camellia pollen offered a further theoretical understanding of its potential applications in preventing and treating nervous system disorders, such as Alzheimer's disease. This study established that Camellia pollen protects the brain against APS-NPs-mediated blood-brain barrier damage and alleviates neuronal apoptosis and Alzheimer's disease-like neurotoxicity. This study elucidates the mechanisms underlying polystyrene-induced brain damage and can be used to inform future prevention and treatment strategies.

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