ArticleFrontiers in pharmacology2025
Nrf2-mediated mechanistic pathways of celastrol nephroprotection: disrupting the oxidative-inflammatory-apoptotic axis in cypermethrin toxicity.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Cypermethrin, a widely used synthetic pyrethroid insecticide, accumulates in renal tissue causing kidney damage through incompletely understood mechanisms. This study evaluated celastrol's nephroprotective effect against cypermethrin-induced kidney injury in rats. Methods: Five groups of male Wistar rats (n = 8 each) received daily treatments for 28 days: control, cypermethrin (25 mg/kg), celastrol (2 mg/kg), and celastrol + cypermethrin at low (1 mg/kg) or high (2 mg/kg) doses. Renal parameters, oxidative stress markers, inflammatory mediators, and apoptotic indicators were assessed using spectrophotometric assays, ELISA, qRT-PCR, and histology. Results: Cypermethrin impaired renal function, increased kidney weight, and elevated Kidney Injury Molecule-1 (KIM-1) levels. It significantly suppressed antioxidant defenses by reducing both the activities and mRNA expression of CAT, SOD, GPx, and GR, alongside GSH depletion and elevated oxidative markers (MDA, NO). Cypermethrin also downregulated the protein and gene expression of Conclusion: Celastrol protects against cypermethrin nephrotoxicity through modulation of antioxidative, anti-inflammatory, and anti-apoptotic mechanisms. Correlation analysis suggests a potential role for Nrf2 in celastrol's integrated nephroprotective effects.
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