We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Dysregulation of the microbiota-brain axis during long-term exposure to polystyrene nanoplastics in rats and the protective role of dihydrocaffeic acid
AI summary Read the abstract
Researchers exposed rats to low doses of polystyrene nanoplastics over 24 weeks and observed disruptions in the gut-brain connection, including changes in gut bacteria, intestinal damage, and altered brain function. A natural compound called dihydrocaffeic acid showed protective effects against these nanoplastic-induced harms. The study suggests that long-term nanoplastic exposure may disrupt the communication between gut microbes and the brain, with potential implications for neurological health.
Polystyrene nano-plastics (PS-NPs) can be accumulated in the food chain and can penetrate biological barriers to affect multiple physiological functions. However, the adverse effects of nano-plastics on mammals and the underlying mechanism still remain unknown. To fill the gaps, our study administrated low-dose PS-NPs (50 and 100 μg/L) for 24 consecutive weeks in rats. Behavioral and morphological evaluations were performed to assess the neurobehavoirs. A combined analysis of multiple omics was used to evaluate the dysfunctions of the gut-microbe-brain axis. After dihydrochalcone(NHDC) treatment in the PS-NPs rat model, the inflammation response and apoptosis process were assessed and proteomics was used to explore the underlying mechanism. Our results indicated that long-term exposure to low-dose PS-NPs could induce abnormal neurobehaviors and amygdaloid nucleus impairment, and stimulate inflammatory responses and apoptosis. Metagenomics results revealed that four microbial phyla including Proteobacteria, Firmicutes, Defferibacteres, and Bacteroidetes changed significantly compared to the control. Targeted metabolomics analysis in the feces showed alteration of 122 metabolites induced by the PS-NPs exposure, among which the content of dihydrocaffeic acid was significantly associated with the different microbial genera and pivotal differential metabolites in the amygdaloid nucleus. And NHDC treatment significantly alleviated PS-NP-induced neuroinflammation and apoptosis and the cyclic adenosine monophosphate(cAMP)/protein kinase A(PKA)/phosphorylated cAMP-response element binding protein(p-CREB)/plasma membrane calcium-transporting ATPase 2(Atp2b2) signaling pathway was identified in the proteomics. In conclusion, long-term exposure to low-dose PS-NPs has adverse effects on emotion through the dysregulation of the gut-brain axis, and dihydrocaffeic acid can alleviate these effects via the cAMP/PKA/p-CREB/Atp2b2 signaling pathway.
More Papers Like This
Intergenerational neurotoxicity of polystyrene nanoplastics in offspring mice is mediated by dysfunctional microbe-gut-brain axis
AI summary Read the abstract
Researchers found that mother mice exposed to polystyrene nanoplastics during pregnancy and nursing passed neurological harm to their offspring, with the babies showing brain inflammation, disrupted dopamine and serotonin signaling, and gut microbiome imbalances — suggesting that nanoplastic exposure before birth can damage the developing brain through the gut-brain connection.
Innovative mechanisms of micro- and nanoplastic-induced brain injury: Emphasis on the microbiota-gut-brain axis
AI summary Read the abstract
This review summarizes how micro- and nanoplastics may damage the brain through the gut-brain axis, a communication pathway between the digestive system and the nervous system. Nanoplastics can disrupt gut bacteria and weaken the intestinal barrier, potentially sending inflammatory signals to the brain. The authors suggest that targeting gut health could be a way to reduce brain damage caused by nanoplastic exposure.
The gut-brain axis involved in polystyrene nanoplastics-induced neurotoxicity via reprogramming the circadian rhythm-related pathways
AI summary Read the abstract
Researchers found that polystyrene nanoplastics given orally to mice crossed the blood-brain barrier and caused neuronal damage in the hippocampus, the brain region responsible for learning and memory. The nanoplastics disrupted the gut-brain connection by altering gut bacteria and circadian rhythm pathways, leading to measurable declines in learning and memory ability. This study provides a biological mechanism showing how ingested plastic nanoparticles could contribute to brain-related health problems in humans.
Long-term exposure to polystyrene microplastics reduces macrophages and affects the microbiota–gut–brain axis in mice
AI summary Read the abstract
Mice that consumed polystyrene microplastics over an extended period showed reduced immune cells called macrophages in their colons and changes in gut bacteria that were linked to altered brain chemistry. This study provides evidence for a gut-brain connection where microplastics may affect brain function indirectly by first disrupting gut health and the immune system.
Therapeutic Benefits of Nano-Echinacea Extract on Reproductive Injury Induced by Polystyrene Plastic Materials in Rat Model via Regulating Gut–Brain Axis
AI summary Read the abstract
Researchers investigated whether nano-formulated Echinacea extract could protect against reproductive damage caused by polystyrene nanoplastics in a rat model. The study found that the nano-Echinacea treatment provided therapeutic benefits against nanoplastic-induced reproductive injury by modulating the gut-brain axis, suggesting that natural plant-based interventions may help counteract some harmful effects of plastic particle exposure.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.