ArticleBMC pharmacology & toxicology2025
Hyperoside mitigates amphotericin B-induced nephrotoxicity in HK-2 cells via bioenergetic and oxidative stress modulation.
Article in BMC pharmacology & toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Hyperoside ameliorates lupus nephritis by suppressing AKT1-mediated PANoptosis in podocytes: integrating network pharmacology and experimental validation.Frontiers in pharmacology · 2025Article
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8 authors.
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Abstract
Amphotericin B (Amp-B/FZ), a first-line antifungal, is limited by dose-dependent nephrotoxicity. This study investigated the protective effects of hyperoside (HP), a dietary flavonoid, against FZ-induced renal toxicity in human proximal tubular (HK-2) cells. Molecular docking revealed strong binding affinities of HP with mitophagy (PINK1/PARKIN) and antioxidant (Nrf2/HO-1) regulators, contrasting with FZ's preferential binding to mitochondrial complex I. FZ (30-60 µM) induced cytotoxicity (MTT/LDH), genotoxicity (comet assay), and bioenergetic disruption: ATP depletion (58%), mitochondrial complex I/III inhibition (42-67%), and PINK1/PARKIN dysregulation. FZ elevated reactive species (3.2-fold) and lipid peroxidation (2.8-fold) while suppressing catalase (64%) and superoxide dismutase (51%) activities. qPCR confirmed FZ-induced downregulation of NDUFS1, CYC1, CAT, and SOD2, alongside impaired Nrf2/HO-1 antioxidant signaling. Co-treatment with HP (20-40 µM) attenuated FZ toxicity, restoring ATP (1.8-fold), mitochondrial complex activities (35-49%), and antioxidant defenses (CAT:2.1-fold, SOD:1.7-fold). HP also normalized Nrf2/HO-1 expression and mitigated oxidative/genotoxic damage. These findings highlight HP's dual role in countering FZ-induced mitochondrial dysfunction and oxidative stress, positioning it as a promising nephroprotective adjuvant. Further in vivo validation could advance HP's clinical application in reducing antifungal-associated renal injury.
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Registered trials
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