ArticleMolecular neurobiology2020
Fucoxanthin Mitigates Subarachnoid Hemorrhage-Induced Oxidative Damage via Sirtuin 1-Dependent Pathway.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- The Role of Reactive Oxygen Species (ROS) in Periodontitis: A Potential Therapeutic Target.Immunity, inflammation and disease · 2025Review
- Brain proteome changes after intracerebral hemorrhage in aged male and female mice.Neurobiology of disease · 2025Article
- Exploring the Role of Ferroptosis-Related Circular RNAs in Subarachnoid Hemorrhage.Molecular biotechnology · 2025Review
- Baihui-Penetrating-Qubin Acupuncture Attenuates Neurological Deficits Through SIRT1/FOXO1 Reducing Oxidative Stress and Neuronal Apoptosis in Intracerebral Hemorrhage Rats.Brain and behavior · 2024Article
- Sirtuins as Potential Targets for Neuroprotection: Mechanisms of Early Brain Injury Induced by Subarachnoid Hemorrhage.Translational stroke research · 2024Review
- Activation of Piezo1 by intracranial hypertension induced neuronal apoptosis via activating hippo pathway.CNS neuroscience & therapeutics · 2024Article
- Antioxidant and Neuroprotective Effects of Fucoxanthin and Its Metabolite Fucoxanthinol: A Comparative In Vitro Study.Current issues in molecular biology · 2024Article
- Fucoxanthin ameliorates traumatic brain injury by suppressing the blood-brain barrier disruption.iScience · 2023Article
- Xanthophyll-Rich Extract ofMolecules (Basel, Switzerland) · 2023Article
- The Critical Role of Sirt1 in Subarachnoid Hemorrhages: Mechanism and Therapeutic Considerations.Brain sciences · 2023Review
- Oxidative Stress and Intracranial Hypertension after Aneurysmal Subarachnoid Hemorrhage.Antioxidants (Basel, Switzerland) · 2022Review
- Brown Algae as Functional Food Source of Fucoxanthin: A Review.Foods (Basel, Switzerland) · 2022Review
- Fucoxanthin Attenuates Oxidative Damage by Activating the Sirt1/Nrf2/HO-1 Signaling Pathway to Protect the Kidney from Ischemia-Reperfusion Injury.Oxidative medicine and cellular longevity · 2022Article
- Activation of SIRT1 Alleviates Ferroptosis in the Early Brain Injury after Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2022Article
- Natural Compounds for SIRT1-Mediated Oxidative Stress and Neuroinflammation in Stroke: A Potential Therapeutic Target in the Future.Oxidative medicine and cellular longevity · 2022Review
- Activation of Sirtuin-1 by Pinocembrin Treatment Contributes to Reduced Early Brain Injury after Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2022Article
- Cycloastragenol Confers Cerebral Protection after Subarachnoid Hemorrhage by Suppressing Oxidative Insults and Neuroinflammation via the SIRT1 Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
- Fucoxanthin Suppresses Osteoclastogenesis via Modulation of MAP Kinase and Nrf2 Signaling.Marine drugs · 2021Article
- SIRT1 Promotes M2 Microglia PolarizationFrontiers in immunology · 2021Article
- Luteolin Confers Cerebroprotection after Subarachnoid Hemorrhage by Suppression of NLPR3 Inflammasome Activation through Nrf2-Dependent Pathway.Oxidative medicine and cellular longevity · 2021Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Oxidative stress is a key component of the pathological cascade in subarachnoid hemorrhage (SAH). Fucoxanthin (Fx) possesses a strong antioxidant property and has shown neuroprotective effects in acute brain injuries such as ischemic stroke and traumatic brain injury. Here, we investigated the beneficial effects of Fx against SAH-induced oxidative insults and the possible molecular mechanisms. Our data showed that Fx could significantly inhibit SAH-induced reactive oxygen species production and lipid peroxidation, and restore the impairment of endogenous antioxidant enzymes activities. In addition, Fx supplementation improved mitochondrial morphology, ameliorated neural apoptosis, and reduced brain edema after SAH. Moreover, Fx administration exerted an improvement in short-term and long-term neurobehavior functions after SAH. Mechanistically, Fx inhibited oxidative damage and brain injury after SAH by deacetylation of forkhead transcription factors of the O class and p53 via sirtuin 1 (Sirt1) activation. EX527, a selective Sirt1 inhibitor, significantly abated Fx-induced Sirt1 activation and abrogated the antioxidant and neuroprotective effects of Fx after SAH. In primary neurons, Fx similarly suppressed oxidative insults and improved cell viability. These effects were associated with Sirt1 activation and were reversed by EX527 treatment. Taken together, our study explored that Fx provided protection against SAH-induced oxidative insults by inducing Sirt1 signaling, indicating that Fx might serve as a potential therapeutic drug for SAH.
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