ArticleInternational urology and nephrology2026
Modulating effects of bee venom (Apis mellifera intermissa) against ethylene glycol-induced oxidative nephrotoxicity in male mice.
Article in International urology and nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeBee venom (BV) is a well-studied nephroprotective agent, however, its efficacy against ethylene glycol (EG)-induced nephrotoxicity has not been previously investigated. Therefore, this study aimed to assess the protective effect of BV in mitigating EG-mediated alterations in renal function markers, oxidative stress, and histopathological injury in male mice.
methodsRenal toxicity was induced in adult male mice by daily oral gavage of 20% EG (2 mL/kg body weight). BV was administered intraperitoneally as a co-treatment over the same exposure period. Evalauted ndpoints included physiological indices (body weight, water intake, urine output, absolute and relative kidney weights), renal filtration markers (serum and urinary urea, creatinine, albumin, and creatinine clearance), urinary electrolytes (Ca
resultsEG administration induced significant systemic and renal impairment, characterized by decreased body weight, increased water intake, urine output, absolute and relative kidney weights, along with reduced creatinine clearance, albuminuria, hypercalciuria, and decreased urinary electrolytes (Na⁺, K⁺, Mg
conclusionBV confers significant but partial nephroprotection against EG-induced oxidative renal injury through suppression of lipid peroxidation, preservation of glutathione status, enhancement of catalase/GST detoxification, and attenuation of tubular and inflammatory damage. These findings support further mechanistic and dose-response optimization studies prior to clinical translation.
Indexed as
Identifiers
42045611What 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.