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Publication
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| Research Title |
Chrysin Ameliorates the Side Effect of Methotrexate Chemotherapy on Antioxidant Status and Neurogenesis in a Rat Model |
| Date of Distribution |
4 May 2023 |
| Conference |
| Title of the Conference |
The 45th Annual Conference of the Anatomy Association of Thailand |
| Organiser |
Department of Anatomy, Faculty of Medicine, Chiang Mai University, Anatomy Association of Thailand (AAT) |
| Conference Place |
Suan Bua Hotel & Resort, Chiang Mai |
| Province/State |
Chiang Mai, Thailand |
| Conference Date |
3 May 2023 |
| To |
5 May 2023 |
| Proceeding Paper |
| Volume |
2023 |
| Issue |
- |
| Page |
20 |
| Editors/edition/publisher |
- |
| Abstract |
Adult neurogenesis is a process of neural stem cell proliferation, migration and differentiation to be newborn neurons. Methotrexate (MTX) is a folic acid antagonist that is widely used as a chemotherapy agent in several types of cancer. However, neurotoxicity of MTX is considerably a major clinical side effect. Chrysin (CH) is a natural flavonoid with various biological properties such as antioxidant and neuroprotective effects. Therefore, the present study was designed to investigate the protective effect of CH against MTX-induced oxidative damage and neurogenesis impairment. Adult Sprague Dawley rats were randomly divided into four groups including vehicle, MTX, CH and MTX+CH groups. Chrysin (10 mg/kg) was administered by oral gavage for 15 days. Intravenous MTX (75 mg/kg) was applied followed by intraperitoneal injection of leucovorin (LCV) on day 8 and 15. The vehicle group received saline, propylene glycol and LCV. Subsequently, the hippocampal neurogenesis was evaluated using Ki67/RECA-1, nestin and Sox2 immunofluorescence staining in the subgranular layer of the dentate gyrus in the hippocampus. Furthermore, the level of oxidative stress marker or malondialdehyde (MDA) and the expression of antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) in the hippocampus and prefrontal cortex were evaluated. The results demonstrated that treatment with CH ameliorated MTX-stimulated neurogenesis impairment by increasing the number of Ki67/RECA-1, nestin and Sox2 positive cells. In addition, CH enhanced the activity of SOD, GPx and CAT enzymes and decreased MDA level in the hippocampus and prefrontal cortex tissues. In conclusion, CH displays neuroprotective effects on MTX-induced neurogenesis impairment via upregulating antioxidant enzyme activity and downregulating oxidative stress. Thus, CH could be a potential therapeutic agent to prevent neurotoxicity of MTX. |
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| Peer Review Status |
ไม่มีผู้ประเมินอิสระ |
| Level of Conference |
ชาติ |
| Type of Proceeding |
Abstract |
| Type of Presentation |
Oral |
| Part of thesis |
true |
| Presentation awarding |
false |
| Attach file |
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| Citation |
0
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Journal Publication
ไทย