ArticleToxics2023
Diosmin Mitigates Gentamicin-Induced Nephrotoxicity in Rats: Insights on miR-21 and -155 Expression, Nrf2/HO-1 and p38-MAPK/NF-κB Pathways.
Article in Toxics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 32 citations in OpenAlex.
- Nano-Diosmin mitigates EAC-induced renal injury through Nrf2-mediated antioxidant activation and NF-κB-dependent apoptotic suppression.Medical oncology (Northwood, London, England) · 2026Article
- Hesperidin attenuates gentamicin-induced nephrotoxicity: Association with SIRT3 and PAX2 expression, oxidative stress, and tubular injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- LC-ESI-TOF-MS profiling and protective effects of Psidium cattleianum extract against gentamicin-induced nephrotoxicity in rats via Nrf2/HO-1 and caspase-dependent pathway.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026Article
- Evaluation of the effects of diosmin in cyclophosphamide-induced nephrotoxicity: an experimental animal study.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Modulation of Oxidative Stress, Inflammation, and Apoptosis and Restoration of Sirt1/Nrf2/HO-1 Signaling by Diosmin Protect Against Diabetes-Induced Testicular Damage in Rats.International journal of molecular sciences · 2026Article
- A novel nanoparticle glutathione and Lepidium sativum treatment for gentamicin-induced acute renal failure in rats.Scientific reports · 2025Article
- Clopidogrel protects against gentamicin-induced nephrotoxicity through targeting oxidative stress, apoptosis, and coagulation pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The spatiotemporal and paradoxical roles of NRF2 in renal toxicity and kidney diseases.Redox biology · 2025Review
- Bee venom ameliorates gentamicin-induced kidney injury by restoring renal aquaporins and enhancing antioxidant and anti-inflammatory activities in rats.Frontiers in pharmacology · 2025Article
- The ameliorative effect of vinpocetine against gentamicin-induced uterine-injury in rats involves the inflammasome/caspase-1/IL-1β pathway.Molecular biology reports · 2024Article
- Connection between Radiation-Regulating Functions of Natural Products and miRNAs Targeting Radiomodulation and Exosome Biogenesis.International journal of molecular sciences · 2023Review
- Parthenolide Phytosomes Attenuated Gentamicin-Induced Nephrotoxicity in Rats via Activation of Sirt-1, Nrf2, OH-1, and NQO1 Axis.Molecules (Basel, Switzerland) · 2023Article
- Renal mitochondrial restoration by gymnemic acid in gentamicin-mediated experimental nephrotoxicity: evidence from serum, kidney and histopathological alterations.Frontiers in pharmacology · 2023Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Gentamicin (GNT) is the most frequently used aminoglycoside. However, its therapeutic efficacy is limited due to nephrotoxicity. Thus, the potential anticipatory effect of Diosmin (DIOS) against GNT-prompted kidney damage in rats together with the putative nephroprotective pathways were scrutinized. Four groups of rats were used: (1) control; (2) GNT only; (3) GNT plus DIOS; and (4) DIOS only. Nephrotoxicity was elucidated, and the microRNA-21 (miR-21) and microRNA-155 (miR-155) expression and Nrf2/HO-1 and p38-MAPK/NF-κB pathways were assessed. GNT provoked an upsurge in the relative kidney weight and serum level of urea, creatinine, and KIM-1. The MDA level was markedly boosted, with a decline in the level of TAC, SOD, HO-1, and Nrf2 expression in the renal tissue. Additionally, GNT exhibited a notable amplification in TNF-α, IL-1β, NF-κB p65, and p38-MAPK kidney levels. Moreover, caspase-3 and BAX expression were elevated, whereas the Bcl-2 level was reduced. Furthermore, GNT resulted in the down-regulation of miR-21 expression along with an up-regulation of the miR-155 expression. Histological examination revealed inflammation, degradation, and necrosis. GNT-provoked pathological abnormalities were reversed by DIOS treatment, which restored normal kidney architecture. Hence, regulating miR-21 and -155 expression and modulating Nrf2/HO-1 and p38-MAPK/NF-κB pathways could take a vital part in mediating the reno-protective effect of DIOS.
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