Melatonin improves hypoxic-ischemic brain damage through the Akt/Nrf2/Gpx4 signaling pathway
| Autor: | Zhixian Gou, Xing Hu, Yue Zhou, Yang Fan, Xiaojuan Su, Liqun Lu, Jing Li, Lin Huang |
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| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine NF-E2-Related Factor 2 Brain damage Pharmacology Hippocampal formation GPX4 Neuroprotection Antioxidants Rats Sprague-Dawley Melatonin 03 medical and health sciences 0302 clinical medicine hemic and lymphatic diseases medicine Animals Ferroptosis Maze Learning neoplasms Protein kinase B Chemistry General Neuroscience Phospholipid Hydroperoxide Glutathione Peroxidase Rats 030104 developmental biology medicine.anatomical_structure Animals Newborn Hypoxia-Ischemia Brain Neuron Signal transduction medicine.symptom Proto-Oncogene Proteins c-akt 030217 neurology & neurosurgery Signal Transduction medicine.drug |
| Zdroj: | Brain Research Bulletin. 163:40-48 |
| ISSN: | 0361-9230 |
| DOI: | 10.1016/j.brainresbull.2020.07.011 |
| Popis: | Melatonin (Mel) has neuroprotective effects; however, its roles in hypoxic-ischemic brain damage (HIBD) and the underlying mechanisms remain unknown. We aimed to explore its roles and mechanisms in a HIBD rat model. We found that exogenous Mel treatment ameliorated HIBD-induced pathological changes, inhibited neuronal ferroptosis, and promoted hippocampal neuronal survival. Moreover, Mel improved the learning and memory abilities of the HIBD rats. Further, we found that glutathione peroxidase 4 (Gpx4) inhibition with RSL3, Akt inhibition with LY29400, and nuclear factor erythroid-2-related factor 2 (Nrf2) inhibition with ML385 abolished the Mel protective effects in HIBD. Our findings indicate that exogenous Mel treatment has a protective effect on HIBD via the Akt/Nrf2/Gpx4 pathway. |
| Databáze: | OpenAIRE |
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