ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Ameliorative effect of rufigallol on cisplatin-induced nephrotoxicity in rats: biochemical and histopathological evaluation.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 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
Abstract
Cisplatin is a prevailing chemotherapeutic drug largely applied for the remedial measure of different types of solid melanoma, having dose-limiting side effects mainly nephrotoxicity and renal failure. Renal failure and nephrotoxicity primarily result from the buildup of cisplatin in renal proximal tubule cells. The toxicity of cisplatin is primarily linked to the generation of reactive oxygen species, which induce oxidative stress and subsequent damage to kidney cells. The present research focused on assessing the regulatory effects of rufigallol (an anthraquinone derivative) on cisplatin-induced nephrotoxicity using various biochemical parameters, oxidative stress markers, pro-inflammatory cytokines, caspase-3, and histopathological assessment. Rats were separated into five test groups, which are Group I: control group (received distilled water for 10 days); Group II: cisplatin (single dose at 5 mg/kg bw, intraperitoneal on 5th day); Groups III and IV: rufigallol (10 and 20 mg/kg bw, respectively, single dose daily for 10 days along with cisplatin 5 mg/kg bw, I.P., once on 5th day); and Group V: rufigallol (alone) (20 mg/kg bw, once in a day for 10 days). The nephrotoxicity produced by cisplatin was addressed by the increased levels of urea, urobilinogen, serum creatinine, urinary proteins, creatinine clearance, urinary KIM-1, serum NGAL, and renal tissue malondialdehyde and nitric oxide levels, as well as decreased levels of serum albumin, superoxide dismutase, catalase, and glutathione in renal tissue. Cisplatin also increased the levels of pro-inflammatory cytokines, inflammatory markers, and tumor markers. Treatment with rufigallol significantly restored nephrotoxicity biomarkers, antioxidant levels, inflammatory cytokines with associated markers, and histopathological damage. Study results indicate that rufigallol may protect against cisplatin-induced nephrotoxicity; however, additional research is needed to confirm its effectiveness in humans.
Indexed as
Identifiers
42776207What Socratic 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 Socratic graph.