ArticleCardiovascular toxicology2026
The Potential Protective Effects of Resveratrol Against Cabazitaxel-Induced Oxidative Stress and Cardiotoxicity in Rats.
Article in Cardiovascular toxicology, 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cabazitaxel, an anti-prostate cancer agent, is associated with dose-dependent cardiotoxicity mediated by oxidative stress. This study investigated cabazitaxel-induced cardiac injury, the utility of intraventricular pressure gradients for early detection, and the potential protective effects of resveratrol. Twenty male Sprague Dawley rats were allocated into four groups: control, therapeutic cabazitaxel (0.5 mg/kg/week, intraperitoneally), toxic cabazitaxel (1.5 mg/kg/week, intraperitoneally), and toxic cabazitaxel + resveratrol (1.5 mg/kg/week cabazitaxel + 10 mg/kg/day resveratrol, intraperitoneally) for 28 days. Cardiac function was assessed via conventional echocardiography, electrocardiography, and intraventricular pressure gradients under anesthesia. Blood samples and heart tissues were collected for further biochemical and histopathological evaluation. Toxic cabazitaxel administration induced significant RR prolongation and bradycardia compared with controls (RR: 0.21 ± 0.02 vs. 0.18 ± 0.02 s; heart rate: 285.88 ± 31.04 vs. 330.40 ± 27.24 bpm), accompanied by aortic dilatation (aortic diameter: 3.73 ± 0.29 vs. 3.28 ± 0.21 mm), reduced acceleration time to ejection time ratio (0.21 ± 0.04 vs. 0.32 ± 0.12), increased derivatives of reactive oxygen metabolites: 394.75 ± 63.47 vs. 324.80 ± 15.56 U.CARR), elevated platelet counts (121.10 ± 26.48 vs. 81.65 ± 6.49 10
Indexed as
Identifiers
What 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.