The gut-brain axis involved in polystyrene nanoplastics-induced neurotoxicity via reprogramming the circadian rhythm-related pathways

Jul 1, 2023Journal of hazardous materials

Gut-brain communication linked to nerve damage from polystyrene nanoplastics through changes in body clock pathways

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Abstract

Mice exposed to 60 μg of 80 nm polystyrene nanoplastics for 42 days showed neuronal damage in the hippocampus.

80 nm polystyrene nanoplastics can penetrate the blood-brain barrier and cause neuronal damage.
Exposure altered the expression of neuroplasticity-related molecules, including serotonin and brain-derived neurotrophic factor.
Learning and memory abilities of the mice were negatively affected by the exposure to nanoplastics.
The gut-brain axis was implicated in the neurotoxic effects, particularly through pathways related to circadian rhythms.
Melatonin and probiotics were effective in reducing intestinal injury and restoring the expression of circadian rhythm-related genes.

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The production of plastic is still increasing globally, which has led to an increasing number of plastic particles in the environment. Nanoplastics (NPs) can penetrate the blood-brain barrier and induce neurotoxicity, but in-depth mechanism and effective protection strategies are lacking. Here, C57BL/6 J mice were treated with 60 μg polystyrene NPs (PS-NPs, 80 nm) by intragastric administration for 42 days to establish NPs exposure model. We found that 80 nm PS-NPs could reach and cause neuronal damage in the hippocampus, and alter the expression of neuroplasticity-related molecules (5-HT, AChE, GABA, BDNF and CREB), and even affect the learning and memory ability of mice. Mechanistically, combined with the results of hippocampus transcriptome, gut microbiota 16 s ribosomal RNA and plasma metabolomics, we found that the gut-brain axis mediated circadian rhythm related pathways were involved in the neurotoxicity of NPs, especially Camk2g, Adcyap1 and Per1 may be the key genes. Both melatonin and probiotic can significantly reduce intestinal injury and restore the expression of circadian rhythm-related genes and neuroplasticity molecules, and the intervention effect of melatonin is more effective. Collectively, the results strongly suggest the gut-brain axis mediated hippocampal circadian rhythm changes involved in the neurotoxicity of PS-NPs. Melatonin or probiotics supplementation may have the application value in the prevention of neurotoxicity of PS-NPs.

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