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61,005 resultsShowing papers similar to Polystyrene microplastics aggravate acute pancreatitis in mice
ClearOral Ingestion of Polystyrene Microplastics Aggravates Chronic Pancreatitis Through ROS Induced NF ‐κb/ TGF ‐β Signaling Pathway and Alteration of Gut Microbiota
Researchers established a chronic pancreatitis mouse model and exposed mice to polystyrene particles of two sizes for 6 weeks, finding that smaller particles caused more severe pancreatic fibrosis, acting through ROS-mediated NF-κB and TGF-β signaling and gut microbiota alteration.
Polystyrene microplastics exacerbate experimental colitis in mice tightly associated with the occurrence of hepatic inflammation
Researchers found that polystyrene microplastics worsened experimentally induced colitis in mice, causing greater intestinal inflammation, reduced mucus secretion, and increased gut permeability. The study also revealed that microplastic exposure in mice with colitis increased the risk of secondary liver inflammation, suggesting that individuals with pre-existing gut conditions may be more vulnerable to microplastic exposure.
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.
Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice
In a mouse study, oral exposure to high concentrations of polystyrene microplastics caused fatty liver disease and abnormal blood lipid levels even without prior gut leakiness. The microplastics triggered intestinal inflammation through immune cells, disrupted gut bacteria, and altered how the body processes nutrients. These results suggest that swallowing microplastics could contribute to metabolic problems and liver disease in humans.
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 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.
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 microplastics aggravate inflammatory damage in mice with intestinal immune imbalance
Researchers found that polystyrene microplastics caused significantly worse inflammatory damage in mice that already had compromised intestinal immune systems compared to healthy mice. The microplastics increased inflammatory markers, disrupted gut bacteria, and caused more severe tissue damage in the vulnerable animals. The study suggests that individuals with pre-existing gut health issues may be more susceptible to the harmful effects of microplastic exposure.
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.
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.
Inflammatory response in the mid colon of ICR mice treated with polystyrene microplastics for two weeks
Researchers found that two weeks of oral polystyrene microplastic exposure in ICR mice induced an inflammatory response specifically in the mid colon, suggesting microplastics may contribute to colonic inflammation.
Hepatic and metabolic outcomes induced by sub-chronic exposure to polystyrene microplastics in mice
Researchers studied the effects of sub-chronic polystyrene microplastic exposure on mouse livers using multiple analytical approaches. They found that microplastics accumulated in liver tissue and caused inflammation, oxidative stress, and disruption of normal metabolic processes including lipid and amino acid metabolism. The study suggests that prolonged microplastic ingestion may pose significant risks to liver health.
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
Microplastic consumption induces inflammatory signatures in the colon and prolongs a viral arthritis
Mice that consumed low doses of polystyrene microplastics showed signs of colon inflammation and experienced prolonged viral arthritis symptoms. The results suggest that microplastic ingestion may worsen inflammatory conditions, though more research is needed to confirm human relevance.
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.
PS-MPs Induced Inflammation and Phosphorylation of Inflammatory Signalling Pathways in Liver
Polystyrene microplastics (0.1 µm) induced inflammatory responses and activated multiple inflammatory signalling pathways in mouse and human liver cell lines after 28 days of exposure. The study identified specific phosphorylation cascades through which PS MPs trigger hepatic inflammation, linking microplastic exposure to liver damage mechanisms.
Influence of Microplastics on Morphological Manifestations of Experimental Acute Colitis
Researchers fed polystyrene microplastics to mice for six weeks and found that healthy mice developed changes in their colon lining, including altered mucus composition and immune cell populations. When mice with experimentally induced colitis also consumed microplastics, their intestinal inflammation was significantly more severe. The study suggests that microplastic exposure may worsen inflammatory bowel conditions.
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.
Chronic environmental exposure to polystyrene microplastics increases the risk of nonalcoholic fatty liver disease
A mouse study found that long-term exposure to polystyrene microplastics increased the risk of developing non-alcoholic fatty liver disease. The microplastics accumulated in the liver and disrupted fat metabolism, causing inflammation and liver damage, which is concerning because most previous studies only looked at short-term exposure effects.
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.
Disruption of hepatic metabolism in Lep KO mice.
Researchers found that polystyrene microplastics administered orally for nine weeks accumulated in liver tissue of leptin-knockout obese mice and induced histopathological liver alterations, including disruption of hepatic lipid, glucose, and amino acid metabolism.
Prolonged oral ingestion of microplastics induced inflammation in the liver tissues of C57BL/6J mice through polarization of macrophages and increased infiltration of natural killer cells
Researchers found that prolonged oral ingestion of polystyrene microplastics caused liver inflammation in mice by polarizing macrophages and increasing natural killer cell infiltration, revealing how microplastics disrupt the liver immune microenvironment.
Polystyrene microplastic exposure induces insulin resistance in mice via dysbacteriosis and pro-inflammation
Researchers found that exposing mice to polystyrene microplastics induced insulin resistance regardless of whether the animals were on a normal or high-fat diet. The study identified disruption of gut bacteria and increased intestinal inflammation as key mechanisms driving the metabolic changes. These findings suggest that microplastic exposure may contribute to metabolic health issues by altering the gut microbiome and triggering chronic inflammation.
Polystyrene microplastics exposure: Disruption of intestinal barrier integrity and hepatic function in infant mice
Researchers found that even low concentrations of polystyrene microplastics caused significant gut barrier damage and liver injury in infant mice. The microplastics disrupted the intestinal lining, allowed particles to leak into the bloodstream, and triggered liver fat accumulation and altered gut bacteria colonization. The study raises concerns about microplastic exposure during early life, when developing digestive and liver systems may be especially vulnerable.