ArticleBrain sciences2023
Protective Effect of Galantamine against Doxorubicin-Induced Neurotoxicity.
Article in Brain sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Unveiling the pathogenesis and therapeutic strategies of Alzheimer's disease through cuproptosis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Attenuation of DOX-Associated Biochemical and Histological Brain Alterations.Veterinary medicine and science · 2026Article
- Repurposing lurasidone to alleviate doxorubicin-induced cardiotoxicity and neurotoxicity via BDNF/TrkB/PI3K/Akt/CREB and miR-34a-5p/PGC-1α pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Sacubitril/valsartan mitigates cisplatin-induced liver injury through modulation of oxidative stress, Caspase-3 activity, and RXR-α signaling in experimental rats.Frontiers in pharmacology · 2026Article
- Sacubitril/Valsartan Fails to Ameliorate Cisplatin-Induced Cognitive Impairment.Drug design, development and therapy · 2026Article
- Galanthamine Fails to Reverse P-gp-Mediated Paclitaxel Resistance in Ovarian Cancer Cell Lines.Biomedicines · 2025Article
- A recent decade update on combating doxorubicin-induced toxicities.Archives of toxicology · 2025Review
- Doxorubicin Toxicity and Recent Approaches to Alleviating Its Adverse Effects with Focus on Oxidative Stress.Molecules (Basel, Switzerland) · 2025Review
- Different Mechanisms in Doxorubicin-Induced Neurotoxicity: Impact of BRCA Mutations.International journal of molecular sciences · 2025Review
- Avenanthramide C mitigates cisplatin-induced hippocampal neurotoxicity and cognitive impairment in rats via suppression of neuroinflammation and neuronal apoptosis.Frontiers in pharmacology · 2025Article
- Protective effects of avenanthramide-C against cisplatin-induced cardiotoxicity in rats by attenuating oxidative stress, inflammatory cytokines, and modulating p62-Keap1-Nrf2 pathway.Frontiers in pharmacology · 2025Article
- Ineffectiveness of tirzepatide in mitigating Doxorubicin-induced oxidative stress and cognitive deficits in a rat model.Frontiers in pharmacology · 2025Article
- Ineffectiveness of pioglitazone in cognitive impairment induced by cyclophosphamide, methotrexate, and fluorouracil via oxidative stress and neuroinflammation.Frontiers in neuroscience · 2025Article
- Ameliorative Effect of Empagliflozin and Linagliptin on Cisplatin-Induced Nephrotoxicity and Cardiotoxicity by Reducing Oxidative Stress.Drug design, development and therapy · 2025Article
- Sacubitril/valsartan fails to prevent doxorubicin-induced cognitive impairment and hippocampal oxidative, inflammatory, and apoptotic alterations in rats.Frontiers in pharmacology · 2025Article
- Neurotoxicity of the antineoplastic drugs: "Doxorubicin" as an example.Journal of molecular histology · 2024Review
- Evaluate the in vitro effect of anthracycline and alkylating cytophosphane chemotherapeutics on dopaminergic neurons.Cancer reports (Hoboken, N.J.) · 2024Article
- LC-MS/MS method for simultaneous Doxorubicin and Baicalein estimation: formulation and pharmacokinetic applications.Nanomedicine (London, England) · 2024Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsDoxorubicin (DOX) causes cognitive impairment (chemobrain) in patients with cancer. While DOX damages the cholinergic system, few studies have focused on the protective effects of cholinergic function on chemobrain. The acetylcholinesterase inhibitor galantamine (GAL) demonstrates neuroprotective properties. We investigated the mechanisms associated with DOX-induced cognitive impairments and the potential protective role of GAL in preventing chemobrain. MAIN
methodsFemale Wistar rats were divided into control, DOX, GAL, and DOX + GAL groups. The rats in the DOX group were administered DOX (5 mg/kg intraperitoneally twice weekly for two weeks), while those in the GAL group were orally administered GAL (2.5 mg/kg) via oral gavage once daily for 15 days. The combination group (DOX + GAL) received GAL (once daily) and DOX (two times per week) concurrently. The body weights and survival rates were monitored daily. The animals were subjected to behavioral tests to assess the memory function followed by the biochemical estimation of inflammatory markers, including tumor necrosis factor-α (TNF- KEY
findingsDOX caused a reduction in the body weight and survival rate, which was alleviated by GAL concomitant treatment with DOX (DOX + GAL). These groups had reduced body weights and survival rates. DOX-treated animals exhibited an impairment of short-term spatial working memory, manifested as a behavioral alteration in the Y-maze test, the novel object recognition (NOR) test, and the elevated plus-maze (EPM) test. Concurrent treatment with GAL (DOX + GAL) showed improved memory function, as evidenced by an increase in the number of entries and time spent in the novel arm, the time spent exploring the novel object, and the transfer latency in the Y-maze, NOR test, and EPM test, respectively. These findings were also supported by biochemical observations showing the reversal of DOX-induced changes in IL-1
conclusionGAL appeared to be a neuroprotective agent against neuroinflammation caused by DOX by reducing inflammatory markers in the brain.
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