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Fasn involved in the nephrotoxicity induced by polystyrene nanoplastics and the intervention of melatonin through intestinal microbiota-mediated lipid metabolism disorder
Summary
Researchers found that polystyrene nanoplastics caused kidney damage in mice, which was linked to disrupted lipid metabolism driven by changes in gut bacteria. They identified a specific pathway involving gut microbes, fatty acid production, and a key metabolic gene that appears to connect intestinal health to kidney injury from nanoplastics. Importantly, the study found that melatonin treatment helped protect the kidneys by restoring healthy lipid metabolism, suggesting a potential preventive approach.
Nanoplastics (NPs) can accumulate in the kidney and cause kidney injury, but the multi-organ interaction mechanism and preventive measures of kidney injury are still unclear. In this study, in vivo (60 µg/day, 42 days) and in vitro (0.4 µg/µL, 24 h) exposure models of polystyrene nanoplastics (PS-NPs, 80 nm) in mice and human kidney cortex proximal tubule epithelial cells (HK-2 cells) were established, respectively. Our study revealed that PS-NPs caused obvious pathological changes and impaired renal function in mice, which were related to lipid metabolism disorders mediated by intestinal flora. Desulfovibrionales-fatty acid synthase (Fasn)-docosahexaenoic acid (DHA) pathway may be one of the mechanisms of kidney injury in mice. Importantly, we also found that melatonin attenuates PS-NPs-induced nephrotoxicity by modulating lipid metabolism disorders (represented by DHA) and affects Fasn expression. In conclusion, our study revealed the important role of intestinal flora-mediated lipid metabolism in PS-NPs-induced nephrotoxicity and preliminarily provided potential key gene targets and effective preventive measures for PS-NPs-induced nephrotoxicity.