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Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen
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Researchers found that polystyrene nanoplastics worsened the inflammatory damage caused by bacterial toxins in the spleens of mice. The nanoplastics triggered oxidative stress that activated inflammatory signaling pathways, leading to cell death, and these effects were significantly amplified when nanoplastics were combined with bacterial endotoxin. The study suggests that nanoplastic exposure may compromise the immune system's ability to handle infections and inflammation.
Plastics are novel environmental pollutants with potential threats to the ecosystem. At least 5.25 trillion plastic particles in the environment, of which nanoplastics are <100 nm in diameter. Polystyrene nanoplastics (PS-NPs) exposure damaged the spleen's immune function. Lipopolysaccharide (LPS) induced other toxicants to damage cells and organs, triggering inflammation. However, the mechanism of PS-NPs aggravated LPS-induced spleen injury remains unclear. In this study, the PS-NPs or/and LPS mice exposure model was replicated by intraperitoneal injection of PS-NPs or/and LPS, and PS-NPs or/and LPS were exposed to RAW264.7 cells. The histopathological and ultrastructural changes of the mice spleen were observed by H&E staining and transmission electron microscope. Western Blot, qRT-PCR, and fluorescent probes staining were used to detect reactive oxygen species (ROS), oxidative stress indicators, inflammatory factors, and necroptosis-related indicators in mice spleen and RAW264.7 cells. The results showed that PS-NPs or LPS induced oxidative stress, activated the MAPK pathway, and eventually caused necroptosis and inflammation in mice spleen and RAW264.7 cells. Compared with the single treatment group, the changes in PS-NPs + LPS group were more obvious. Furthermore, ROS inhibitor N-Acetyl-L-cysteine (NAC) significantly inhibited the activation of the mitogen-activated protein kinase (MAPK) signaling pathway caused by co-treatment of PS-NPs and LPS, reducing necroptosis and inflammation. The results demonstrated that PS-NPs promoted LPS-induced spleen necroptosis and inflammation in mice through the ROS/MAPK pathway. This study increases the data on the damage of PS-NPs to the organism and expands the research ideas and clues.
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Polystyrene nanoplastics deteriorate LPS-modulated duodenal permeability and inflammation in mice via ROS drived-NF-κB/NLRP3 pathway
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Researchers found that polystyrene nanoplastics worsened intestinal inflammation and increased gut permeability in mice already exposed to bacterial endotoxin. The combined exposure triggered higher levels of oxidative stress and activated inflammatory pathways, leading to greater damage to the intestinal lining than either substance alone. The study suggests that nanoplastic exposure could make the gut more vulnerable to inflammation and barrier breakdown when other stressors are present.
Surface functionalization-dependent inflammatory potential of polystyrene nanoplastics through the activation of MAPK/ NF-κB signaling pathways in macrophage Raw 264.7
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Researchers studied how surface chemistry of polystyrene nanoplastics affects their ability to trigger inflammation in immune cells. They found that amino-functionalized nanoplastics caused the strongest inflammatory response by activating the MAPK and NF-kB signaling pathways and generating reactive oxygen species. The study demonstrates that the chemical coating on nanoplastics significantly determines their potential to cause immune system disruption.
Polystyrene nanoplastics aggravates lipopolysaccharide‐induced apoptosis in mouse kidney cells by regulating IRE1/XBP1 endoplasmic reticulum stress pathway via oxidative stress
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Researchers investigated whether polystyrene nanoplastics could worsen kidney cell damage caused by bacterial toxins in mice. They found that nanoplastics aggravated cell death by triggering oxidative stress, which activated a specific endoplasmic reticulum stress pathway involving the IRE1/XBP1 signaling cascade. The study suggests that combined exposure to nanoplastics and bacterial compounds may pose greater risks to kidney health than either stressor alone.
Polystyrene nanoplastics exacerbate lipopolysaccharide-induced myocardial fibrosis and autophagy in mice via ROS/TGF-β1/Smad
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Researchers found that polystyrene nanoplastics worsened heart damage in mice already exposed to bacterial toxins, accelerating scarring and disrupting normal heart tissue maintenance. The combined exposure triggered increased oxidative stress and activated a specific signaling pathway linked to tissue fibrosis. The study suggests that nanoplastic exposure could amplify existing cardiac stress, potentially compounding heart problems when the body is already under inflammatory challenge.
Table 1_Polystyrene nanoplastics induce oxidative stress in Aurelia coerulea polyps, microglia, and mice.docx
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Researchers investigated oxidative stress responses to polystyrene nanoplastics in three model systems—jellyfish polyps, BV2 microglia, and ICR mice—and found activation of the MAPK signalling pathway across all models. In mice, NP exposure also produced neurobehavioural changes, strengthening evidence for neurological effects of polystyrene nanoplastic exposure.
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