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61,005 resultsShowing papers similar to Oral Ingestion of Polystyrene Microplastics Aggravates Chronic Pancreatitis Through ROS Induced NF ‐κb/ TGF ‐β Signaling Pathway and Alteration of Gut Microbiota
ClearPolystyrene microplastics aggravate acute pancreatitis in mice
Researchers found that polystyrene microplastics aggravated acute pancreatitis in mice by amplifying inflammatory responses, with exposure at 100 and 1000 micrograms per liter worsening pancreatic damage induced by cerulein injection.
Polystyrene microplastics induced inflammation with activating the TLR2 signal by excessive accumulation of ROS in hepatopancreas of carp (Cyprinus carpio)
Researchers exposed carp to polystyrene microplastics and found that the particles induced inflammation in the hepatopancreas by triggering excessive accumulation of reactive oxygen species and activating the TLR2 immune signaling pathway. Both tissue-level and cellular experiments confirmed increased expression of inflammatory molecules including TNF-alpha and IL-1beta. The study reveals a specific molecular mechanism by which microplastics cause inflammatory damage in freshwater fish organs.
Polystyrene micro- and nanoplastics induce gastric toxicity through ROS mediated oxidative stress and P62/Keap1/Nrf2 pathway
In a mouse study, polystyrene micro and nanoplastics at environmentally relevant doses caused significant stomach damage, including reduced gastric juice and mucus production, weakened stomach barrier function, and increased oxidative stress. The damage was driven by reactive oxygen species triggering a specific cell-signaling pathway that led to cell death. This research suggests that microplastics in food and water could harm stomach health, an organ that gets first exposure when contaminated food is consumed.
Polystyrene nanoplastics induce intestinal and hepatic inflammation through activation of NF-κB/NLRP3 pathways and related gut-liver axis in mice
In a mouse study, ingested polystyrene nanoplastics accumulated in the gut and liver and triggered inflammation through specific immune pathways, damaging the intestinal lining and allowing bacterial toxins to leak into the liver. This gut-liver connection suggests that swallowing nanoplastics could set off a chain reaction of inflammation affecting multiple organs in the body.
Polystyrene nanoplastics deteriorate LPS-modulated duodenal permeability and inflammation in mice via ROS drived-NF-κB/NLRP3 pathway
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.
Polystyrene microplastics-induced macrophage extracellular traps contributes to liver fibrotic injury by activating ROS/TGF-β/Smad2/3 signaling axis
In a mouse study, polystyrene microplastics caused liver scarring (fibrosis) by triggering immune cells called macrophages to release web-like traps that promoted inflammation. Smaller microplastic particles caused more severe liver damage than larger ones, and the damage involved a specific signaling pathway (ROS/TGF-beta/Smad2/3) that drives tissue scarring. This research reveals a new mechanism by which microplastics may contribute to chronic liver disease.
Polystyrene microplastics trigger colonic inflammation in rats via the TLR4/NF-κB/COX-2 pathway and modulation of intestinal microbiota
Rats exposed to polystyrene microplastics for 90 days developed significant colon inflammation, including damaged gut lining, increased inflammatory markers, and disrupted gut bacteria. The study identified a specific inflammatory pathway (TLR4/NF-kB/COX-2) through which microplastics trigger intestinal inflammation, providing important clues about how plastic particles in food and water could contribute to gut diseases in humans.
Polystyrene nanoplastics induce glycolipid metabolism disorder via NF-κB and MAPK signaling pathway in mice
Researchers fed mice polystyrene nanoplastics and found that the particles disrupted the animals' ability to regulate blood sugar and fat metabolism. The nanoplastics triggered oxidative stress and inflammation in the liver, activating signaling pathways that led to insulin resistance and abnormal fat accumulation. The study provides evidence that nanoplastic exposure may contribute to metabolic disorders through specific molecular mechanisms involving the NF-kB and MAPK pathways.
PS-MPs promotes the progression of inflammation and fibrosis in diabetic nephropathy through NLRP3/Caspase-1 and TGF-β1/Smad2/3 signaling pathways.
In a mouse model of diabetic nephropathy, polystyrene microplastic exposure worsened kidney inflammation and fibrosis by activating the NLRP3/Caspase-1 and TGF-beta1/Smad2/3 signaling pathways, suggesting microplastics may accelerate progression of this common diabetic complication.
Polystyrene micro- and nanoplastics aggravates colitis in a mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
Researchers found that polystyrene micro- and nanoplastics aggravated colitis symptoms in a mouse model, increasing gut permeability, inflammatory cytokine levels, and tissue damage compared to controls. The study provides mechanistic evidence linking microplastic exposure to worsening of inflammatory bowel conditions.
Polystyrene micro- and nanoplastics in a colitis mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
Researchers exposed colitis mouse models to polystyrene micro- and nanoplastics to test whether MNP exposure worsens inflammatory bowel disease, finding that MNPs altered biodistribution and exacerbated inflammatory responses in animals with pre-existing gut inflammation.
Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen
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.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
Immune response to polystyrene microplastics: Regulation of inflammatory response via the ROS-driven NF-κB pathway in zebrafish (Danio rerio)
Researchers found that polystyrene microplastics triggered immune system inflammation in zebrafish by generating reactive oxygen species (ROS) that activated the NF-kB signaling pathway. The microplastics accumulated mainly in the intestines, causing tissue damage and behavioral changes in the fish. This study identifies a specific molecular mechanism by which microplastics cause immune dysfunction, which could be relevant to understanding inflammation in humans exposed to microplastics.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
PET microplastics increase the risk of insulin resistance and pancreatitis
Researchers fed young piglets PET microplastics for four weeks and found significant metabolic changes in their pancreatic tissue, including disrupted fat metabolism and signs of inflammation. Piglets receiving the higher dose showed tissue changes consistent with early pancreatitis, and both dose groups showed markers associated with insulin resistance. The study suggests that microplastic exposure in developing organisms may affect pancreatic function, though more research is needed to understand implications for humans.
Negative impact of oral exposure to polystyrene microplastics on glucose tolerance and intestinal environment in mice is independent of particle size
Researchers fed mice on a high-fat diet polystyrene microplastics of three different sizes and found that all sizes impaired glucose tolerance, regardless of particle dimensions. The microplastics caused intestinal inflammation, altered gut bacteria, and damaged the lining of the intestinal tract. The study suggests that the harmful metabolic effects of ingesting microplastics may occur broadly and are not limited to one particular particle size.
The role of gut microbiota in mediating increased toxicity of nano-sized polystyrene compared to micro-sized polystyrene in mice
This mouse study found that nano-sized polystyrene plastics were significantly more toxic than micro-sized ones, causing greater gut inflammation, liver damage, and metabolic disruption. The key difference was driven by how each size affected gut bacteria: nanoplastics caused a more severe shift toward harmful bacteria and away from beneficial ones. The findings suggest that the smallest plastic particles may pose the greatest health risk because they more dramatically disrupt the gut microbiome.
Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.
A long-term mouse study examined how chronic exposure to polystyrene microspheres interacts with a high-fat diet to affect obesity-related outcomes, finding that microplastics worsened metabolic disruption and fat accumulation compared to diet alone. The results raise concern that microplastic exposure may be an environmental factor contributing to the global obesity epidemic.
Polystyrene Microplastics Exacerbate Systemic Inflammation in High-Fat Diet-Induced Obesity
Researchers found that polystyrene microplastics significantly worsened inflammation and metabolic problems in obese mice fed a high-fat diet. The microplastics were found throughout the body including the brain, where they activated immune cells in the hypothalamus, a region that controls appetite and metabolism. This study suggests that microplastic exposure could be an overlooked factor contributing to the worsening of obesity-related health problems like insulin resistance and chronic inflammation.
Long-term exposure to polystyrene microplastics promotes HFD-induced obesity in mice through exacerbating microbiota dysbiosis
Researchers found that long-term polystyrene microplastic exposure worsened high-fat-diet-induced obesity in mice by exacerbating gut microbiota dysbiosis, suggesting microplastic ingestion may amplify metabolic disease risk through disruption of the gut microbiome.
Size-dependent toxicity of polystyrene microplastics on the gastrointestinal tract: Oxidative stress related-DNA damage and potential carcinogenicity
Researchers found that polystyrene microplastics accumulate mainly in stomach tissue, where smaller nanoscale particles cause more severe damage than larger ones. The nanoplastics reduced antioxidant enzyme activity, increased DNA damage markers, and activated signaling pathways associated with cancer development. These size-dependent effects on the gastrointestinal tract suggest that the smallest plastic particles may pose the greatest risk to digestive health.
A Western-style diet shapes the gut and liver responses to low-dose, fit-for-purpose polystyrene nanoplastics in mice
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.
Proinflammatory properties and lipid disturbance of polystyrene microplastics in the livers of mice with acute colitis
Researchers studied the effects of polystyrene microplastics on the livers of mice fed a high-fat diet and found that the particles triggered significant inflammatory responses and disrupted lipid metabolism. The microplastics worsened fat accumulation in the liver and activated inflammatory signaling pathways. The findings suggest that microplastic exposure combined with a high-fat diet may amplify liver damage and metabolic disturbances.