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Papers
61,005 resultsShowing papers similar to Therapeutic potential of Ganoderma lucidum polysaccharide peptide in Doxorubicin-induced nephropathy: modulation of renin-angiotensin system and proteinuria
ClearGalangin attenuates oxidative stress-mediated apoptosis in high glucose-induced renal tubular epithelial cells through modulating renin–angiotensin system and PI3K/AKT/mTOR pathway
Researchers found that a plant compound called galangin protected kidney cells from damage caused by high blood sugar by reducing oxidative stress and activating protective signaling pathways. While focused on diabetes treatment, this research is not directly related to microplastic contamination.
Attenuative Effects of Ginkgetin Against Polystyrene Microplastics-Induced Renal Toxicity in Rats
Researchers found that ginkgetin, a natural flavonoid, significantly reduced polystyrene microplastic-induced kidney damage in rats by restoring antioxidant enzyme activity and reducing oxidative stress and inflammation markers.
Sotagliflozin prevents acute kidney injury by suppressing oxidative stress, inflammation, and apoptosis in renal ischemia/reperfusion rat model
This study found that sotagliflozin, a dual SGLT1/2 inhibitor, protects against acute kidney injury in rats by reducing oxidative stress, inflammation, and cell death in a renal ischemia/reperfusion model. While not directly about microplastics, the study is relevant to understanding kidney protection mechanisms, as microplastics have been detected in kidney tissue and may contribute to renal inflammation.
Pharmacological assessment of delphinidin in counteracting polystyrene microplastic induced renal dysfunction in rats
Researchers investigated whether the plant compound delphinidin could protect against kidney damage caused by polystyrene microplastics in rats. They found that microplastic exposure triggered oxidative stress, inflammation, and cell death markers in kidney tissue, while delphinidin treatment significantly restored normal kidney function. The study suggests that delphinidin may have protective properties against microplastic-induced organ damage in animal models.
STS Protects Diabetic Glomerular Vascular Endothelial Barrier by Ameliorating EPC Dysfunction: Targeting RAGE-TXNIP-NLRP3 Inflammasome Pathway
This study investigated how a compound called STS (Sodium Tanshinone IIA Sulfonate) protects kidney blood vessels in diabetic kidney disease by targeting an inflammatory pathway. STS helped repair endothelial progenitor cells that are damaged by diabetes, reducing kidney injury. This paper is focused on a therapeutic mechanism in diabetes and is not directly related to microplastics.
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.
Evaluation of Possible Ameliorative Role of Robinetin to Counteract Polystyrene Microplastics Instigated Renal Toxicity in Rats
Researchers tested whether robinetin, a plant-derived compound, could protect rat kidneys from damage caused by polystyrene microplastic exposure. They found that microplastics caused significant kidney harm through oxidative stress, inflammation, and cell death, but robinetin supplementation substantially reversed these effects. The study suggests that natural antioxidant compounds may offer a protective strategy against microplastic-related organ damage.
Toxicological effects of microplastics in renal ischemia–reperfusion injury
Researchers studied how microplastic exposure affects kidney injury and recovery in a mouse model of reduced blood flow to the kidneys. They found that microplastics worsened kidney damage by triggering inflammatory responses and disrupting cellular repair processes. The study suggests that microplastic accumulation in the body may increase vulnerability to kidney complications.
Microparticles as Potential Mediators of High Glucose-Induced Renal Cell Injury.
This study investigates the role of microparticles — small vesicles shed by cells — in kidney disease progression under high-glucose conditions, testing their involvement in cellular stress pathways relevant to diabetic nephropathy. The paper uses 'microparticles' to refer to cell-derived vesicles rather than environmental plastic particles, and is not related to plastic pollution.
Ameliorative Effects of Rhamnetin against Polystyrene Microplastics-Induced Nephrotoxicity in Rats
Researchers investigated whether the flavonoid rhamnetin could protect against kidney damage caused by polystyrene microplastics in rats. The study found that microplastic exposure significantly increased oxidative stress and inflammatory markers while reducing antioxidant enzyme activity, but co-treatment with rhamnetin restored kidney parameters and mitigated the damage.
Sakuranetin counteracts polyethylene microplastics induced nephrotoxic effects via modulation of Nrf2/Keap1 pathway
Researchers found that polyethylene microplastics caused kidney damage in rats by increasing oxidative stress and disrupting a key protective cellular pathway. However, when the natural plant compound sakuranetin was administered alongside the microplastics, it significantly reduced the kidney damage by restoring antioxidant defenses. The study suggests that certain natural compounds may help counteract some of the harmful effects of microplastic exposure on organ health.
Effects of nano- and microplastics on kidney: Physicochemical properties, bioaccumulation, oxidative stress and immunoreaction
Researchers exposed mice to polystyrene nano- and microplastics of varying sizes and tracked their accumulation and effects in the kidneys. They found that the particles changed their physical properties during digestion, accumulated in kidney tissue, and caused oxidative stress and immune responses. The study suggests that plastic particle size plays an important role in determining the extent of kidney-related harm.
Protective Effect of Resveratrol on Kidney Disease and Hypertension Against Microplastics Exposure in Male Juvenile Rats
Researchers investigated whether resveratrol, a natural plant compound, could protect young rats from kidney damage and high blood pressure caused by microplastic exposure. They found that microplastics elevated blood pressure and creatinine levels through oxidative stress, and that resveratrol treatment effectively prevented these effects. The study suggests resveratrol may offer protective benefits against organ damage linked to microplastic exposure, partly by improving gut microbiota balance.
Effects of Microplastic (MP) Exposure at Environmentally Relevant Doses on the Structure, Function, and Transcriptome of the Kidney in Mice
Researchers exposed mice to polystyrene microplastics at doses matching levels found in the environment and examined the effects on kidney structure and function. While the microplastics did not cause obvious physical damage to the kidneys, they altered blood markers of kidney function and changed gene expression patterns related to immune response and metabolism. The study suggests that even low-level microplastic exposure may subtly affect kidney biology at the molecular level.
Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
Researchers co-exposed rats to polystyrene nanoplastics and the antibiotic gentamicin and found that the combination caused significantly greater kidney damage than either substance alone, amplifying oxidative stress, inflammation, and mitochondrial apoptosis in a synergistic manner.
Microplastic exposure and its consequences for renal and urinary health: systematic review of in vivo studies
This systematic review examines animal studies on how microplastic exposure affects the kidneys and urinary system. The evidence suggests that microplastics can accumulate in kidney tissue and may cause inflammation and oxidative stress, raising concerns about potential long-term effects on human kidney health as our exposure to these particles continues to grow.
Polystyrene microplastics facilitate renal fibrosis through accelerating tubular epithelial cell senescence
Mice exposed to polystyrene microplastics at doses relevant to human exposure developed kidney inflammation and scarring (fibrosis) within 28 days. The microplastics caused kidney tube cells to age prematurely, triggering a chain reaction that activated scar-forming cells through a specific signaling pathway. This study provides evidence that microplastic exposure could contribute to chronic kidney damage in people.
Postbiotic Sodium Butyrate Mitigates Hypertension and Kidney Dysfunction in Juvenile Rats Exposed to Microplastics
This study reports that sodium butyrate, a postbiotic compound, mitigated microplastic-induced hypertension and kidney dysfunction in juvenile rats by reducing oxidative stress, modulating the gut microbiota, and elevating butyric acid levels.
Microplastiques : une menace silencieuse pour vos reins ?
Researchers reviewed evidence on microplastic contamination and its potential effects on kidney health, noting that microplastics have been detected in kidneys and urine in humans. In vitro and animal studies suggest potential nephrotoxicity from microplastic exposure, and patients with kidney diseases may face increased risk due to higher exposure through medical procedures and reduced urinary elimination. The study calls for further research to clarify the relationship between microplastic exposure and kidney damage.
Resveratrol Butyrate Esters Reduce Hypertension in a Juvenile Rat Model of Chronic Kidney Disease Exacerbated by Microplastics
Researchers found that resveratrol butyrate esters reduced high blood pressure in young rats that had both chronic kidney disease and microplastic exposure. The protective effects worked by improving nitric oxide levels, regulating the body's blood pressure control system, and positively shifting gut bacteria composition. The study suggests that certain natural compounds may help counteract the cardiovascular harm associated with microplastic exposure.
Research progress on damage-associated molecular patterns in acute kidney injury
This review explores how damage-associated molecular patterns (DAMPs), molecules released by injured cells, drive inflammation in acute kidney injury. The authors note that environmental stressors including microplastics can trigger DAMP release, which activates immune pathways that worsen kidney damage. Understanding these molecular mechanisms could lead to new therapeutic strategies for preventing kidney injury progression.
The microplastics exposure induce the kidney injury in mice revealed by RNA-seq
In a mouse study, microplastics of different sizes caused kidney injury including inflammation, oxidative stress, and scarring (fibrosis) after long-term exposure. The smallest particles (80 nanometers) altered immune-related genes, while larger particles disrupted genes tied to the body's internal clock. This research provides evidence that microplastics accumulating in the body over time could contribute to kidney disease in mammals, including humans.
Microplastics and CKD: Are we overlooking the role of ecotoxins
This review argues that microplastics deserve greater consideration as a contributing factor to chronic kidney disease, synthesizing evidence that MPs can accumulate in renal tissue, trigger inflammation and oxidative stress, and may represent an underappreciated environmental driver of CKD.
Polystyrene microplastic-induced extracellular vesicles cause kidney-related effects in the crosstalk between tubular cells and fibroblasts
Researchers found that polystyrene microplastics cause kidney tubule cells to release tiny signaling packages (extracellular vesicles) that trigger stress responses and scarring in neighboring kidney cells. This cell-to-cell communication pathway spread the damage beyond the cells directly exposed to the microplastics. The findings suggest a mechanism by which microplastic exposure could contribute to kidney fibrosis and long-term kidney damage in humans.