ArticleOncotarget2017
Neuroprotective effect of a novel gastrodin derivative against ischemic brain injury: involvement of peroxiredoxin and TLR4 signaling inhibition.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Natural herbal extract roles and mechanisms in treating cerebral ischemia: A systematic review.Frontiers in pharmacology · 2024Pooled it
- Peroxiredoxins in Stroke: Friends and Foes.Cells · 2026Review
- Peroxiredoxins in central nervous system: implications for chronic pain and anaesthetic-induced neurotoxicity management.Redox biology · 2025Review
- A review: Mechanism and prospect of gastrodin in prevention and treatment of T2DM and COVID-19.Heliyon · 2023Review
- FreshFrontiers in pharmacology · 2023Article
- Gastrodin Alleviates Acetaminophen-Induced Liver Injury in a Mouse Model Through Inhibiting MAPK and Enhancing Nrf2 Pathways.Inflammation · 2022Article
- Changing Perspectives from Oxidative Stress to Redox Signaling-Extracellular Redox Control in Translational Medicine.Antioxidants (Basel, Switzerland) · 2022Review
- Role of DAMPs and of Leukocytes Infiltration in Ischemic Stroke: Insights from Animal Models and Translation to the Human Disease.Cellular and molecular neurobiology · 2022Review
- Gastrodin and Vascular Dementia: Advances and Current Perspectives.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Phthalide derivative CD21 attenuates tissue plasminogen activator-induced hemorrhagic transformation in ischemic stroke by enhancing macrophage scavenger receptor 1-mediated DAMP (peroxiredoxin 1) clearance.Journal of neuroinflammation · 2021Article
- Neuroprotective Effect of Phthalide Derivative CD21 against Ischemic Brain Injury:Involvement of MSR1 Mediated DAMP peroxiredoxin1 Clearance and TLR4 Signaling Inhibition.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- Effects of Peroxiredoxin 2 in Neurological Disorders: A Review of its Molecular Mechanisms.Neurochemical research · 2020Review
- Intracerebral Hemorrhage-Induced Brain Injury in Rats: the Role of Extracellular Peroxiredoxin 2.Translational stroke research · 2020Article
- Enhancement of neural stem cell survival, proliferation and differentiation by IGF-1 delivery in graphene oxide-incorporated PLGA electrospun nanofibrous mats.RSC advances · 2019Article
- Reactive Oxygen Species Formation in the Brain at Different Oxygen Levels: The Role of Hypoxia Inducible Factors.Frontiers in cell and developmental biology · 2018Review
- Danger signals in stroke and their role on microglia activation after ischemia.Therapeutic advances in neurological disorders · 2018Review
- Protective Effect of Klotho against Ischemic Brain Injury Is Associated with Inhibition of RIG-I/NF-κB Signaling.Frontiers in pharmacology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inhibition of extracellular inflammatory peroxiredoxin (Prx) signaling appears to be a potential therapeutic strategy for neuroinflammatory injury after acute ischemic stroke. Gastrodin (Gas) is a phenolic glycoside that is used for the treatment of cerebral ischemia, accompanied by regulation of the autoimmune inflammatory response. The present study investigated the neuroprotective effects of Gas and its derivative, Gas-D, with a focus on the potential mechanism associated with inflammatory Prx-Toll-like receptor 4 (TLR4) signaling. Gas-D significantly inhibited Prx1-, Prx2-, and Prx4-induced inflammatory responses in RAW264.7 macrophages and H2O2-mediated oxidative injury in SH-SY5Y nerve cells. In rats, intraperitoneal Gas-D administration 10 h after reperfusion following 2-h middle cerebral artery occlusion (MCAO) ameliorated neurological deficits, brain infarction, and neuropathological alterations, including neuron loss, astrocyte and microglia/macrophage activation, T-lymphocyte invasion, and lipid peroxidation. Delayed Gas-D treatment significantly inhibited postischemic Prx1/2/4 expression and spillage, TLR4 signaling activation, and inflammatory mediator production. In contrast, Gas had no significant effects in either cell model or in MCAO rats under the same conditions. These results indicate that Gas-D may be a drug candidate with an extended therapeutic time window that blocks inflammatory responses and attenuates the expression and secretome of inflammatory Prxs in acute ischemic stroke.
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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.