ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Protective effects of taxifolin against gentamicin-induced nephrotoxicity in mice: modulation of oxidative stress, inflammation, apoptosis, and Nrf2 signaling.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Hesperidin attenuates gentamicin-induced nephrotoxicity: Association with SIRT3 and PAX2 expression, oxidative stress, and tubular injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Effects of ATP and Taxifolin on Atezolizumab-Induced Renal Injury: A Biochemical, Histopathological, and Immunofluorescence Evaluation.Life (Basel, Switzerland) · 2026Article
- Renoprotective effects of vitamin D and thymoquinone, alone and in combination, in a rat co-treatment model of gentamicin-induced acute kidney injury.Molecular and cellular biochemistry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gentamicin (GEN), an antibiotic belonging to aminoglycosides, is commonly administered to treat gram-negative bacterial infections. However, GEN nephrotoxicity restricts its therapeutic applications. The study examined the nephroprotective efficiency of a plant flavonoid (Taxifolin, TX) against GEN-associated renal damage in mice. Oral administration of TX (25 or 50 mg/kg/day) in mice for 14 days was followed by intraperitoneal GEN (100 mg/kg/day) treatments from the 8th to 14th day. GEN-treated mice were characterized by higher creatinine and urea levels in the serum and significant renal histopathological modifications. They also presented elevated malondialdehyde (MDA) and protein carbonyl and decreased levels of reduced glutathione (GSH) and activities of catalase (CAT), and superoxide dismutase (SOD). TX effectively improved renal function and antioxidant potential while simultaneously lowering MDA and protein carbonyl levels in GEN-administered mice. Furthermore, TX suppressed the renal expressions of nuclear factor kappa B (NF-κB) p65 and decreased levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in GEN-treated mice. GEN treatment increased caspase-3 and Bcl-2 associated X (Bax) and reduced B-cell lymphoma-2 (Bcl-2) protein levels in mouse kidneys. These effects were significantly mitigated by TX treatment. GEN administration significantly suppressed nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) protein levels in mouse kidneys. Largely, TX restored renal Nrf2 and HO-1 protein levels, as evidenced by immunohistochemistry and ELISA analyses, respectively, in GEN-treated mice. Overall, TX provided nephroprotection against GEN-induced kidney damage via modulation of oxidative stress, inflammation, and apoptosis and restoration of Nrf2 signaling. Thus, TX could be a promising adjuvant candidate to prevent drug-linked organ injury.
Indexed as
Identifiers
40580310What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.