ArticleIranian journal of medical sciences2017
Protective Effect of Edaravone Against Cyclosporine-Induced Chronic Nephropathy Through Antioxidant and Nitric Oxide Modulating Pathways in Rats.
Article in Iranian journal of medical sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Edaravone Mitigates Di(2-ethylhexyl) Phthalate-Induced Nephrotoxicity Through Attenuation of Oxidative Stress and Endoplasmic Reticulum Stress.Journal of biochemical and molecular toxicology · 2026Article
- Pre-Exposure to Cyclosporine A Primes Paracoccidioides brasiliensis to Evade Host Immunity.ACS infectious diseases · 2026Article
- Cyclosporine-induced kidney damage was halted by sitagliptin and hesperidin via increasing Nrf2 and suppressing TNF-α, NF-κB, and Bax.Scientific reports · 2024Article
- Evaluation of the protective effect of edaravone on doxorubicin nephrotoxicity by [Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis.Molecular medicine reports · 2018Article
- Self-nanomicellizing solid dispersion of edaravone: part I - oral bioavailability improvement.Drug design, development and therapy · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCyclosporine A (CsA) is an immunosuppressant with therapeutic indications in various immunological diseases; however, its use is associated with chronic nephropathy. Oxidative stress has a crucial role in CsA-induced nephrotoxicity. The present study evaluates the protective effect of edaravone on CsA-induced chronic nephropathy and investigates its antioxidant and nitric oxide modulating property.
methodsMale Sprague-Dawley rats (n=66) were distributed into nine groups, including a control (group 1) (n=7). Eight groups received CsA (15 mg/kg) for 28 days while being treated. The groups were categorized as: Group 2: Vehicle (n=10)Groups 3, 4, and 5: Edaravone (1, 5, and 10 mg/kg) (n=7 each)Group 6: Diphenyliodonium chloride, a specific endothelial nitric oxide synthase (eNOS) inhibitor (n=7)Group 7: Aminoguanidine, a specific inducible nitric oxide synthase (iNOS) inhibitor (n=7)Group 8: Edaravone (10 mg/kg) plus diphenyliodonium chloride (n=7)Group 9: Edaravone (10 mg/kg) plus aminoguanidine (n=7) Blood urea nitrogen and serum creatinine levels, malondialdehyde, superoxide dismutase, and glutathione reductase enzyme activities were measured using standard kits. Renal histopathological evaluations and measurements of eNOS and iNOS gene expressions by RT-PCR were also performed. Data were analyzed using one-way analysis of variance (ANOVA) followed by Tukey's test (SPSS software version 18.0).
resultsEdaravone (10 mg/kg) significantly attenuated CsA-induced oxidative stress, renal dysfunction, and kidney tissue injury. Aminoguanidine improved the renoprotective effect of edaravone. Edaravone reduced the elevated mRNA level of iNOS, but could not alter the level of eNOS mRNA significantly.
conclusionEdaravone protects against CsA-induced chronic nephropathy using antioxidant property and probably through inhibiting iNOS gene expression.
Indexed as
Identifiers
28360443PMC5366365W2587096690What OpenQuestion holds
Registered trials
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