ArticleMolecular biology reports2025
The pantothenic acid derivative dexpanthenol ameliorated doxorubicin-induced neurotoxicity via regulating AKT/CREB/BDNF and AKT/NRF2 signaling pathways.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Dexpanthenol Attenuates Doxorubicin-Induced Cardiotoxicity by Modulating Oxidative Stress, Inflammation, and Apoptosis.Cardiovascular toxicology · 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
Abstract
backgroundDoxorubicin (Dox)-induced neurotoxicity is a well-documented side effect of chemotherapy. Dexpanthenol (Dex), an analog of vitamin B5, has shown protective properties. This study aimed to explore the molecular mechanisms by which Dex mitigates Dox-induced neurotoxicity, particularly through the protein kinase B (AKT)/cyclic AMP-response element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) pathway and nuclear factor erythroid 2-related factor 2 (NRF2) signaling. METHODS AND
resultsThe experiment was conducted using four groups: control, Dex, Dox, and Dox + Dex, comprising a total of 32 female Wistar Albino rats. After two weeks of treatment, the rats were euthanized, and brain and cerebellum tissues were collected for analysis. Biochemical analysis was performed spectrophotometrically to assess oxidative stress parameters, while histological and immunostaining analyses focused on nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) immunoexpressions. Genetic analysis of AKT, CREB, BDNF, and NRF2 gene expressions was conducted using real-time polymerase chain reaction. Histopathological evaluation of the Dox group revealed hyperemia, microhemorrhage, neuronal damage, and neuronophagia. Additionally, an increase in caspase-3, tumor necrosis factor-alpha, NF-κB, and iNOS immunoexpressions were observed, along with elevated total oxidant status and oxidative stress index. A decrease in AKT, CREB, BDNF, and NRF2 gene expressions accompanied these changes. Dex treatment significantly reversed these pathological findings, effectively protecting the brain from Dox-induced neuronal damage.
conclusionIn conclusion, Dex may provide neuroprotection in female rats with Dox-induced neurotoxicity by activating the CREB/BDNF pathway and reducing oxidative stress through AKT-mediated NRF2 synthesis. Further detailed studies exploring additional pathways are required to incorporate Dex into cancer treatment protocols and minimize side effects.
Indexed as
Identifiers
39945917What 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.