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Promising protective potential of MiR-103a-3p against polystyrene microplastic neurotoxicity in rats
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Researchers discovered that a small molecule called miR-103a-3p can protect rat brains from the damage caused by polystyrene microplastics. When injected into the brain, miR-103a-3p reversed the learning and memory problems caused by microplastic exposure by reducing inflammation, oxidative stress, and cell death in the hippocampus. This finding points toward potential therapeutic strategies for counteracting the brain-damaging effects of microplastic exposure.
Introduction: Microplastics are ubiquitous environmental pollutants with potential neurotoxic effects that can impair learning and memory. MicroRNAs are essential regulators of a number of physiological and pathological processes, but detailed information on the impact of miRNAs on the neurotoxic effects of microplastics is lacking. Methods: In the present study, polystyrene microplastics (PS-MPs) were administered orally and miR-103a-3p was injected intracerebroventricularly as a treatment for PS-MPs-induced neurotoxicity. Results and Discussion: Performance in the novel object discrimination Y-maze and Barnes maze tests indicated that miR-103a-3p mitigates the deleterious effects of PS-MPs on learning and memory. Oxidative stress, pyroptosis, apoptosis and inflammation induced by PS-MPs were modulated after miR- 103a-3p injection by reducing malondialdehyde, protein carbonyl, nitrite, caspase 3, caspase 1, TNFα, and NLRP3 levels in hippocampal tissue. Our results also showed that miR-103a-3p can reverse the impact of PS-MPs on astrocytic reaction and SIRT1 and BDNF levels. MiR-103a-3p alleviated PS-MPs-induced endoplasmic reticulum (ER) stress through reducing the levels of PERK, CHOP and GRP78. These findings imply that miR-103a-3p exerts a neuroprotective influence against cognitive deficits induced by exposure to PS-MPs. This is achieved by reducing inflammation, oxidative stress, apoptosis and endoplasmic reticulum stress.
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MiR‐532‐5p Attenuates Cognitive Deficits and Endoplasmic Reticulum Stress Subsequent to Polystyrene Microplastics
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Researchers investigated whether microRNA miR-532-5p mediates cognitive and memory deficits caused by polystyrene microplastics and found that PS-MP exposure downregulated miR-532-5p in the brain, impairing learning and memory via endoplasmic reticulum stress pathways. Restoring miR-532-5p levels attenuated cognitive deficits, identifying it as a potential therapeutic target for microplastic-induced neurotoxicity.
Evaluation of Neurotoxicity in BALB/c Mice following Chronic Exposure to Polystyrene Microplastics
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Researchers found that chronic exposure to polystyrene microplastics in mice led to learning and memory problems along with signs of neurotoxicity. The study suggests that long-term microplastic exposure may impair brain function in mammals. These findings raise important questions about the potential neurological risks of microplastic exposure for the broader public.
Targeted activation of ErbB4 receptor ameliorates neuronal deficits and neuroinflammation in a food-borne polystyrene microplastic exposed mouse model
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In mice exposed to polystyrene microplastics through food, researchers found significant brain inflammation and cognitive problems, but activating a specific brain receptor (ErbB4) with a small molecule drug helped reverse these effects. This suggests that microplastic exposure through diet may contribute to brain damage, and points toward possible treatments for microplastic-related neurological harm.
Neurotoxic effects of polystyrene nanoplastics on memory and microglial activation: Insights from in vivo and in vitro studies
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In a mouse study, tiny nanoplastics (30-50 nanometers) that were swallowed reached the brain and caused memory problems by activating the brain's immune cells, called microglia, which triggered inflammation. This is concerning because it shows that nanoplastics small enough to be found in everyday products like cosmetics could cross into the brain and impair cognitive function.
Polystyrene microplastics induce auditory neurotoxicity in mammals: Integrated multi-omics profiling reveals oxidative damage and synaptic molecular dysregulation
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In rats, tiny plastic particles called microplastics were found to travel to the brain's hearing centers and disrupt how neurons communicate, causing damage that showed up in brain processing before it affected the ears themselves. The plastics triggered harmful oxidative stress and interfered with a key cell signaling pathway, but researchers found that boosting this pathway could help protect brain cells from the damage. While this study was done in rats, not humans, it raises important questions about whether the microplastics we're constantly exposed to in food, water, and air could affect our hearing and brain health.
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