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Salvianolic acid B attenuates cholesterol dysregulation induced by polystyrene nanoplastics
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In mice fed tiny plastic particles called nanoplastics for 28 days, liver cholesterol buildup, inflammation and other changes occurred. A plant compound called Salvianolic acid B, given for 14 days, reduced liver cholesterol and some related changes but did not restore all measured markers to normal, in both mice and lab-grown immune cells.
Micro- and nanoplastics are associated with metabolic toxicity, but their effects on hepatic cholesterol homeostasis and potential mitigating interventions remain insufficiently characterized. To characterize hepatic responses to 50-nm PS-NPs and determine whether Sal B modulates these responses. In a 28-day oral exposure model, PS-NPs consistently increased hepatic cholesterol and produced focal lipid deposition, localized histological alterations, F4/80-positive macrophage enrichment, and increased ROS. These changes were accompanied by increased SREBF1, p62/SQSTM1, NF-κB, and COX2 abundance and reduced PPARA and other PPAR-related proteins. In a separate 14-day intervention model, Sal B reduced hepatic cholesterol and focal lipid deposition and modulated CD36-, SREBF1-, and PPAR-related proteins, although aminotransferases and representative inflammatory lipid mediators were not broadly restored. Docking predicted favorable interactions of Sal B with CD36 and COX2. In THP-1-derived macrophages, Sal B reduced PS-NP-induced CD36 elevation and increased JC-1 red fluorescence without a significant change in the red/green ratio. PS-NPs produced a cholesterol-centered hepatic metabolic phenotype, and Sal B selectively attenuated lipid-related and associated molecular responses rather than uniformly normalizing the broader biochemical profile.
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Sinensetin mitigates polystyrene nanoplastics induced hepatotoxicity in albino rats: A biochemical and histopathological study
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Exposure to polystyrene nanoplastics caused significant liver damage in rats, including oxidative stress, inflammation, and cell death, along with elevated liver enzymes that are markers of liver injury in clinical settings. Treatment with sinensetin — a natural plant flavonoid — substantially reversed these effects, restoring antioxidant enzyme activity and reducing inflammatory markers. The findings establish a potential protective role for natural compounds against nanoplastic-induced organ toxicity and illuminate the mechanisms by which nanoplastics harm the liver.
Long-term polystyrene nanoplastic exposure disrupt hepatic lipid metabolism and cause atherosclerosis in ApoE-/- mice
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Long-term exposure to tiny polystyrene nanoplastics caused atherosclerosis (hardening of the arteries) in mice by disrupting fat metabolism in the liver and triggering inflammation and oxidative stress. This is one of the first studies to directly link nanoplastic exposure to cardiovascular disease development, raising concerns about heart health risks from the nanoplastics found in our food and environment.
Chronic Polystyrene Nanoplastics Exposure Reprograms Gene Expression, Alternative Splicing, and Disrupts Host–Microbiome–Metabolic Networks to Promote Atherosclerosis in LDLr⁻/⁻ Mice
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Tiny plastic particles (nanoplastics), similar in size to what's already been found in human arteries, made clogged-artery disease significantly worse in mice by disrupting liver function, altering gut bacteria, and throwing off protective body chemicals—all at the same time. This matters because these mice were genetically similar to how many people process cholesterol, and the same disease patterns showed up when researchers compared their data to human artery disease samples, suggesting everyday plastic exposure could be a hidden contributor to heart disease risk in people, too.
Surface chemistry and size-related particle attributes shape lipidomic responses to polystyrene micro- and nanoplastics in zebrafish liver cells
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Zebrafish liver cells in a lab test were exposed to tiny plastic particles of different sizes and surface coatings. Particles coated with an amino group changed cholesterol-related fats and lowered a related gene's activity, while plain nanoplastics altered certain membrane fats, showing that particle surface chemistry and size affect cell fat composition.
A Western-style diet shapes the gut and liver responses to low-dose, fit-for-purpose polystyrene nanoplastics in mice
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A subchronic mouse study found that low-dose polystyrene nanoplastics designed to mimic real-world particle characteristics impaired gut and liver health in a non-monotonic, diet-dependent manner, with Western-style diet amplifying the effects.
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