ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Melatonin Treatment Regulates SIRT3 Expression in Early Brain Injury (EBI) Due to Reactive Oxygen Species (ROS) in a Mouse Model of Subarachnoid Hemorrhage (SAH).
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 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Perspectives on Alzheimer's Disease Treatment Based on Counteracting Oxidative Stress.Biomolecules · 2025Review
- Melatonin-A Powerful Antioxidant in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Nimodipine ameliorates subarachnoid hemorrhage-induced neuroinflammation and injury by protecting mitochondrial function and regulating autophagy.Human cell · 2025Article
- Improving anti-oxidant stress treatment of subarachnoid hemorrhage through self-assembled nanoparticles of oleanolic acid.Drug delivery · 2024Article
- Sirtuins as Potential Targets for Neuroprotection: Mechanisms of Early Brain Injury Induced by Subarachnoid Hemorrhage.Translational stroke research · 2024Review
- Depression like-behavior and memory loss induced by methylglyoxal is associated with tryptophan depletion and oxidative stress: a new in vivo model of neurodegeneration.Biological research · 2024Article
- New Insights of Early Brain Injury after Subarachnoid Hemorrhage: A Focus on the Caspase Family.Current neuropharmacology · 2023Article
- Role of SIRT3 in neurological diseases and rehabilitation training.Metabolic brain disease · 2023Review
- Sirtuin-3: A potential target for treating several types of brain injury.Frontiers in cell and developmental biology · 2023Review
- Melatonin as an Antioxidant Agent in Stroke: An Updated Review.Aging and disease · 2022Review
- Redox Biology of Melatonin: Discriminating Between Circadian and Noncircadian Functions.Antioxidants & redox signaling · 2022Review
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Melatonin as a Potential Neuroprotectant: Mechanisms in Subarachnoid Hemorrhage-Induced Early Brain Injury.Frontiers in aging neuroscience · 2022Review
- Inflammation and immune cell abnormalities in intracranial aneurysm subarachnoid hemorrhage (SAH): Relevant signaling pathways and therapeutic strategies.Frontiers in immunology · 2022Review
- Multi-omics landscape of circadian rhythm pathway alterations in Glioma.Bioengineered · 2021Article
- Glutamate, Glutamine, GABA and Oxidative Products in the Pons Following Cortical Injury and Their Role in Motor Functional Recovery.Neurochemical research · 2021Article
- The cellular immunotherapy of integrated photothermal anti-oxidation Pd-Se nanoparticles in inhibition of the macrophage inflammatory response in rheumatoid arthritis.Acta pharmaceutica Sinica. B · 2021Article
- Inhibition of Ferroptosis Alleviates Early Brain Injury After Subarachnoid Hemorrhage In Vitro and In Vivo via Reduction of Lipid Peroxidation.Cellular and molecular neurobiology · 2021Article
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND A mouse model of subarachnoid hemorrhage (SAH) investigated the effects of melatonin treatment on the generation of reactive oxygen species (ROS) and the activation of the SIRT3 gene in early brain injury (EBI). MATERIAL AND METHODS Male C57BL/6J mice were assigned to three groups: the SAH group; the sham group; and the SAH + melatonin-treated group (intraperitoneal dose, 150 mg/kg). TUNEL was used to study apoptosis of neuronal cells, Western-blot and immunohistochemistry detected expression of Sirt3, Bcl-2, superoxide dismutase 2 (SOD2), Bax, and cleaved caspase-3. Real-time polymerase chain reaction (PCR) and a luciferase reporter assay evaluated the effects of melatonin on SIRT3 gene expression. Malondialdehyde (MDA) and the reactive oxygen species (ROS) scavenger, reduced glutathione (GSH), and its ratio with oxidized glutathione (GSSG) was measured. RESULTS The increase in neurological score and increase in cerebral edema following SAH were reduced in the SAH + melatonin-treated group. Neuronal apoptosis following SAH was reduced in the SAH + melatonin-treated group. Increased levels of SOD2, Bax, and cleaved caspase-3 following SAH were reduced in the SAH + melatonin-treated group; reduced levels of Sirt3 and Bcl-2 following SAH were increased in the SAH + melatonin-treated group. The GSH: GSSG ratio was increased, and the MDA level was decreased when melatonin treatment was used following SAH. Melatonin upregulated SIRT3 expression by increasing the transcription efficiency of the SIRT3 promoter in human glioma cell lines U87 and U251. CONCLUSIONS Melatonin provided protection from the effects of EBI following SAH by regulating the expression of murine SIRT3.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.