دورية أكاديمية
Galantamine mitigates neurotoxicity caused by doxorubicin via reduced neuroinflammation, oxidative stress, and apoptosis in rat model.
| العنوان: | Galantamine mitigates neurotoxicity caused by doxorubicin via reduced neuroinflammation, oxidative stress, and apoptosis in rat model. |
|---|---|
| المؤلفون: | Aldubayan MA; Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Buraydah, Al Qassim, Saudi Arabia. aalhowail@qu.edu.sa., Alsharidah AS, Alenezi SK, Alhowail AH |
| المصدر: | European review for medical and pharmacological sciences [Eur Rev Med Pharmacol Sci] 2024 Jan; Vol. 28 (2), pp. 805-813. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Verduci Country of Publication: Italy NLM ID: 9717360 Publication Model: Print Cited Medium: Internet ISSN: 2284-0729 (Electronic) Linking ISSN: 11283602 NLM ISO Abbreviation: Eur Rev Med Pharmacol Sci Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Rome : Verduci, [1997- |
| مواضيع طبية MeSH: | Galantamine*/pharmacology , NF-kappa B*/metabolism, Rats ; Animals ; Caspase 3/metabolism ; bcl-2-Associated X Protein/metabolism ; Neuroinflammatory Diseases ; Cyclooxygenase 2/metabolism ; Oxidative Stress ; Doxorubicin/toxicity ; Glutathione/metabolism ; Apoptosis ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Superoxide Dismutase/metabolism |
| مستخلص: | Objective: Doxorubicin (DXR) is commonly used as a drug for cancer treatment. However, there have been reports of neurotoxicity associated with chemotherapy. Galantamine (GLN) is a medication that inhibits cholinesterase activity, providing relief from the neurotoxic effects commonly seen in individuals with Alzheimer's disease. This study explored the potential ameliorative effect of GLN on brain neurotoxicity induced by DXR. Materials and Methods: Forty rats were allocated into four separate groups for a study that lasted for a period of fourteen days. The control group was given normal saline, DXR group was given 5 mg/kg DXR every three days (cumulative dose of 20 mg/kg) through intraperitoneal injection. The GLN group was given 5 mg/kg GLN through oral gavage daily, while the DXR+GLN group was given DXR+GLN simultaneously. An analysis of brain proteins using ELISA to assess apoptosis through the concentration of inflammation and oxidative injury markers. Results: The DXR treatment led to increased neuroinflammation by elevation of nuclear factor kappa B (NF-κB), and cyclooxygenase-2 (COX-2), oxidative stress by rise of malondialdehyde (MDA), and decline of superoxide dismutase (SOD), and no changes in catalase and glutathione (GSH), cell death by elevation of Bax and caspase-3 and reduced Bcl-2, and increase lipid peroxidation, impaired mitochondrial function. When GLN is administered alongside DXR, it has been observed to positively impact various biological markers, including COX-2, NF-κB, MDA, SOD, Bax, Bcl-2, and caspase-3 levels. Additionally, GLN improves lipid peroxidation and mitochondrial activity. Conclusions: DXR therapy in rats results in the development of neurotoxicity, and a combination of GLN can recover these toxicities, suggesting GLN promising evidence for mitigating the neurotoxic effects induced by DXR. |
| المشرفين على المادة: | 0D3Q044KCA (Galantamine) EC 3.4.22.- (Caspase 3) 0 (bcl-2-Associated X Protein) 0 (NF-kappa B) EC 1.14.99.1 (Cyclooxygenase 2) 80168379AG (Doxorubicin) GAN16C9B8O (Glutathione) 0 (Proto-Oncogene Proteins c-bcl-2) EC 1.15.1.1 (Superoxide Dismutase) |
| تواريخ الأحداث: | Date Created: 20240202 Date Completed: 20240205 Latest Revision: 20240205 |
| رمز التحديث: | 20240205 |
| DOI: | 10.26355/eurrev_202401_35081 |
| PMID: | 38305623 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 2284-0729 |
|---|---|
| DOI: | 10.26355/eurrev_202401_35081 |