ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Melatonin Upregulates Nuclear Factor Erythroid-2 Related Factor 2 (Nrf2) and Mediates Mitophagy to Protect Against Early Brain Injury After Subarachnoid Hemorrhage.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Unraveling the role of mitochondrial dysfunction in diabetic kidney disease: insights and interventions.Frontiers in pharmacology · 2025Review
- Therapeutic utility of Perfluorocarbon Oxygent in limiting the severity of subarachnoid hemorrhage in mice.Scientific reports · 2024Article
- Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage.Neural regeneration research · 2024Review
- Mitochondrial stress: a key role of neuroinflammation in stroke.Journal of neuroinflammation · 2024Review
- Effect of Nrf2 on brain injury induced by hydraulic shock via regulation of mitophagy and apoptosis.Aging · 2023Article
- Melatonin delivered in solid lipid nanoparticles ameliorated its neuroprotective effects in cerebral ischemia.Heliyon · 2023Article
- Melatonin as an Antioxidant Agent in Stroke: An Updated Review.Aging and disease · 2022Review
- Mitophagy and reactive oxygen species interplay in Parkinson's disease.NPJ Parkinson's disease · 2022Review
- Melatonin Alleviates Neonatal Necrotizing Enterocolitis by Repressing the Activation of the NLRP3 Inflammasome.Gastroenterology research and practice · 2022Article
- Melatonin as a Potential Neuroprotectant: Mechanisms in Subarachnoid Hemorrhage-Induced Early Brain Injury.Frontiers in aging neuroscience · 2022Review
- New Mechanisms and Targets of Subarachnoid Hemorrhage: A Focus on Mitochondria.Current neuropharmacology · 2022Review
- ACEA Attenuates Oxidative Stress by Promoting Mitophagy via CB1R/Nrf1/PINK1 Pathway after Subarachnoid Hemorrhage in Rats.Oxidative medicine and cellular longevity · 2022Article
- Role of Mitophagy in the Pathogenesis of Stroke: From Mechanism to Therapy.Oxidative medicine and cellular longevity · 2022Review
- Neuroprotective Effects of Early Brain Injury after Subarachnoid Hemorrhage in Rats by Calcium Channel Mediating Hydrogen Sulfide.Cellular and molecular neurobiology · 2021Article
- Selective autophagy as a therapeutic target for neurological diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Antioxidants and Neuron-Astrocyte Interplay in Brain Physiology: Melatonin, a Neighbor to Rely on.Neurochemical research · 2021Review
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
- Phytochemicals Bridging Autophagy Induction and Alpha-Synuclein Degradation in Parkinsonism.International journal of molecular sciences · 2019Review
- CD28 Deficiency Ameliorates Thoracic Blast Exposure-Induced Oxidative Stress and Apoptosis in the Brain through the PI3K/Nrf2/Keap1 Signaling Pathway.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The aim of this study was to investigate whether melatonin is involved in brain injury following subarachnoid hemorrhage (SAH). MATERIAL AND METHODS An SAH model was established and TUNEL assays were utilized to detect the effect of melatonin on cell apoptosis. Western blot analysis was used to detect the effect of melatonin on expression of autophagic markers and apoptotic factors. Real-time PCR, Western blot analysis, and luciferase assay were performed to study the effect of melatonin on nuclear factor erythroid-2 related factor 2 (NRF2) expression. RESULTS The SAH group displayed a lower neurological score and a higher brain water content, while melatonin treatment increased the neurological score and decreased the brain water content. The administration of melatonin also inhibited the apoptosis of neurons in the brain. In addition, higher Beclin-1 expression and higher conversion ratio from LC3- II to LC3-I were observed in the SAH group. The activation of Beclin-1 and the conversion from LC3-II to LC3-I was further enhanced by melatonin treatment. Furthermore, in the SAH group, the level of Bcl-2 was decreased while the level of Bax and cleaved caspase-3 were increased. However, following melatonin treatment in the SAH group, the level of Bcl-2 was increased while the levels of Bax and cleaved caspase-3 were decreased. CONCLUSIONS Our study indicated that, by increasing the expression of NRF2, the mitophagy induced by melatonin provided protection against brain injury post-SAH.
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