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61,005 resultsShowing papers similar to STS Protects Diabetic Glomerular Vascular Endothelial Barrier by Ameliorating EPC Dysfunction: Targeting RAGE-TXNIP-NLRP3 Inflammasome Pathway
ClearSodium tanshinone IIA sulfonate ameliorates neointima by protecting endothelial progenitor cells in diabetic mice
Researchers found that a compound called sodium tanshinone IIA sulfonate (STS) protected blood vessel repair cells (endothelial progenitor cells) in diabetic mice, reducing harmful artery wall thickening by blocking an inflammation pathway. This suggests STS may help prevent cardiovascular complications linked to diabetes-related vascular damage.
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.
Galangin 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.
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.
Therapeutic potential of Ganoderma lucidum polysaccharide peptide in Doxorubicin-induced nephropathy: modulation of renin-angiotensin system and proteinuria
This paper is not directly about microplastics — it evaluates a polysaccharide peptide from Ganoderma lucidum mushroom as a treatment for doxorubicin-induced kidney injury in mice, finding it inhibits the renin-angiotensin system and reduces proteinuria.
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.
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.
SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction
Researchers found that nanoplastics cause premature aging and dysfunction in blood vessel lining cells, and that an SGLT2 inhibitor drug could help counteract these effects. The nanoplastics triggered oxidative stress and inflammation in endothelial cells, which are linked to cardiovascular problems. The study suggests a potential therapeutic approach to address some of the vascular damage associated with nanoplastic exposure.
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.
Narirutin ameliorates polystyrene microplastics induced nephrotoxicity by modulating oxidative stress, inflammation and Nrf2/Keap1 pathway
Researchers investigated whether narirutin, a natural compound found in citrus fruits, could protect kidneys from damage caused by polystyrene microplastics in rats. The study suggests that microplastic exposure triggered significant kidney stress through oxidation and inflammation, but narirutin helped reduce that damage by activating protective cellular pathways.
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.
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.
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.
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.
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.
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.
Acute kidney injury: exploring endoplasmic reticulum stress-mediated cell death
This review examines how endoplasmic reticulum stress, a cellular response to accumulated misfolded proteins, can trigger various forms of cell death in acute kidney injury. While not directly about microplastics, these same stress pathways are activated when cells are exposed to nanoplastics, which have been shown to accumulate in kidney tissue. Understanding these mechanisms helps explain how microplastic exposure could contribute to kidney damage at the cellular level.
Exposure to Nanoplastics Induces an Inflammatory Response in Healthy and Type 2 Diabetic Primary Human Proximal Tubular Epithelial Cells
This conference abstract reports that nanoplastic exposure triggers inflammatory responses in human kidney (proximal tubular) cells, with the response being stronger in cells from donors with type 2 diabetes. The finding is significant because it suggests that people with pre-existing metabolic conditions may be more vulnerable to the cellular damage caused by nanoplastics, which can reach the kidneys after ingestion.
Polystyrene microplastics induced nephrotoxicity associated with oxidative stress, inflammation, and endoplasmic reticulum stress in juvenile rats
This study found that polystyrene microplastics caused kidney damage in young rats through a combination of oxidative stress, inflammation, and a cellular stress response called endoplasmic reticulum stress. The microplastics also reduced body weight growth and affected multiple organs including the heart and ovaries. These findings suggest that microplastic exposure during development could be particularly harmful to kidney health in young, growing organisms.
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.
Issue Information‐ToC
This brief notice indicates a paper in the journal issue that examines how polystyrene nanoplastics worsen inflammation-triggered cell death (apoptosis) in mouse kidney cells exposed to bacterial toxins. The interaction between nanoplastics and inflammatory signals may amplify kidney damage beyond what either stressor alone would cause.
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.
Network toxicology and bioinformatics analysis reveal the molecular mechanisms of polyethylene terephthalate microplastics in exacerbating diabetic nephropathy
This computational study used bioinformatics to explore how polyethylene terephthalate (PET) microplastics might worsen diabetic kidney disease. The analysis identified key genes and inflammatory pathways that are affected by both PET microplastics and kidney damage in diabetes. The findings suggest that microplastic exposure could accelerate kidney problems in people who already have diabetes, though lab and clinical studies are needed to confirm this.
Peptide Extract from Apricot Kernels Mitigates Damage in Human Aortic Endothelial Cells Induced by Polystyrene Microplastics through theInhibition of the NLRP3 Signaling Pathway
Researchers found that a peptide extract from apricot kernels protects human aortic endothelial cells from polystyrene microplastic-induced damage by simultaneously suppressing NLRP3 inflammasome activation and reducing oxidative stress through Wnt/β-catenin pathway inhibition, reducing apoptosis by 39.1% and inflammatory cytokines by 17–38%.