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Curcumin attenuates nanoparticle-induced renal injury via the PI3K/AKT signaling pathway
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Curcumin was found to protect kidney cells from polystyrene nanoplastic-induced injury by activating the PI3K/AKT signaling pathway, demonstrated through both in vitro and in vivo experiments using network pharmacology. This is significant for microplastic pollution research as it identifies a potential natural therapeutic intervention against the nephrotoxic effects of nanoplastic exposure.
Exposure to polystyrene nanoplastics (PS-NPs) endangers human health, so exploring curcumin (Cur)'s nephroprotective effects against PS-NPs-induced injury is crucial. This research integrated network pharmacology with in vitro and in vivo...
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Polystyrene nanoplastics and lung cancer: Insights from network toxicology and mechanistic in vitro studies
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Network toxicology analysis identified 189 potential molecular targets linking polystyrene nanoplastic exposure to lung cancer pathways, and in vitro experiments confirmed that nanoplastics promote lung cancer cell proliferation and resistance to apoptosis via PI3K/AKT signaling.
Screening for polystyrene nanoparticle toxicity on kidneys of adult male albino rats using histopathological, biochemical, and molecular examination results
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Researchers found that oral exposure to polystyrene nanoparticles caused significant kidney damage in rats, including oxidative stress, impaired renal function, and tissue alterations that worsened with increasing dose, demonstrating their nephrotoxic potential.
Polystyrene nanoplastics induce apoptosis of human kidney proximal tubular epithelial cells via oxidative stress and MAPK signaling pathways
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Researchers found that polystyrene nanoplastics cause programmed cell death in human kidney tubular cells through oxidative stress and activation of the MAPK signaling pathway. The toxic effects were dependent on both the size and dose of the nanoplastics, with smaller particles causing more damage. The study identifies specific molecular mechanisms by which nanoplastics may contribute to kidney cell injury.
Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
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Researchers co-exposed rats to polystyrene nanoplastics and the antibiotic gentamicin and found that the combination caused significantly greater kidney damage than either substance alone, amplifying oxidative stress, inflammation, and mitochondrial apoptosis in a synergistic manner.
Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys
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Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.