ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2015
Epigallocatechin-3-Gallate (EGCG) Attenuates Traumatic Brain Injury by Inhibition of Edema Formation and Oxidative Stress.
Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
- Clinical insights into catechin-based nanomedicine: a review of therapeutic potential in neurodegenerative diseases.3 Biotech · 2025Review
- Epigallocatechin 3-gallate-induced neuroprotection in neurodegenerative diseases: molecular mechanisms and clinical insights.Molecular and cellular biochemistry · 2025Review
- Epigallocatechin-3-gallate therapeutic potential in human diseases: molecular mechanisms and clinical studies.Molecular biomedicine · 2024Review
- Tanshinone IIA attenuates fluoride-induced spinal cord injury by inhibiting ferroptosis and inflammation.Heliyon · 2024Article
- J147 treatment protects against traumatic brain injury by inhibiting neuronal endoplasmic reticulum stress potentially via the AMPK/SREBP-1 pathway.Translational research : the journal of laboratory and clinical medicine · 2024Article
- Neutrophil Targeting Platform Reduces Neutrophil Extracellular Traps for Improved Traumatic Brain Injury and Stroke Theranostics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Risk factors and predictive model of cerebral edema after road traffic accidents-related traumatic brain injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2024Article
- Catechin Protects against Lipopolysaccharide-induced Depressive-like Behaviour in Mice by Regulating Neuronal and Inflammatory Genes.Current gene therapy · 2024Article
- Aquaporin 4 in Traumatic Brain Injury: From Molecular Pathways to Therapeutic Target.Neurochemical research · 2022Review
- A comprehensive review of the influence of Epigallocatechin gallate on Sjögren's syndrome associated molecular regulators of exocytosis (Review).Biomedical reports · 2021Review
- Intracisternal administration of tanshinone IIA-loaded nanoparticles leads to reduced tissue injury and functional deficits in a porcine model of ischemic stroke.IBRO neuroscience reports · 2021Article
- The Emerging Roles of Antioxidant Enzymes by Dietary Phytochemicals in Vascular Diseases.Life (Basel, Switzerland) · 2021Review
- (-)-Epigallocatechin-3-gallate provides neuroprotection via AMPK activation against traumatic brain injury in a mouse model.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Green tea catechins inhibit microglial activation which prevents the development of neurological disorders.Neural regeneration research · 2020Review
- Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions.Biomedicines · 2020Review
- The Attenuation of Traumatic Brain Injury via Inhibition of Oxidative Stress and Apoptosis by Tanshinone IIA.Oxidative medicine and cellular longevity · 2020Article
- Preparation and Evaluation of Recombinant Human Erythropoietin Loaded Tween 80-Albumin Nanoparticle for Traumatic Brain Injury Treatment.International journal of nanomedicine · 2020Article
- NADPH oxidases in traumatic brain injury - Promising therapeutic targets?Redox biology · 2018Review
- Epigallocatechin Gallate Attenuates Bladder Dysfunction via Suppression of Oxidative Stress in a Rat Model of Partial Bladder Outlet Obstruction.Oxidative medicine and cellular longevity · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a major cause of mortality and long-term disability, which can decrease quality of life. In spite of numerous studies suggesting that Epigallocatechin-3-gallate (EGCG) has been used as a therapeutic agent for a broad range of disorders, the effect of EGCG on TBI remains unknown. In this study, a weight drop model was established to evaluate the therapeutic potential of EGCG on TBI. Rats were administered with 100 mg/kg EGCG or PBS intraperitoneally. At different times following trauma, rats were sacrificed for analysis. It was found that EGCG (100 mg/kg, i.p.) treatment significantly reduced brain water content and vascular permeability at 12, 24, 48, 72 hour after TBI. Real-time PCR results revealed that EGCG inhibited TBI-induced IL-1β and TNF-α mRNA expression. Importantly, CD68 mRNA expression decreasing in the brain suggested that EGCG inhibited microglia activation. Western blotting and immunohistochemistry results showed that administering of EGCG significantly inhibited the levels of aquaporin-4 (AQP4) and glial fibrillary acidic protein (GFAP) expression. TBI-induced oxidative stress was remarkably impaired by EGCG treatment, which elevated the activities of SOD and GSH-PX. Conversely, EGCG significantly reduced the contents of MDA after TBI. In addition, EGCG decreased TBI-induced NADPH oxidase activation through inhibition of p47(phox) translocation from cytoplasm to plasma membrane. These data demonstrate that EGCG treatment may be an effective therapeutic strategy for TBI and the underlying mechanism involves inhibition of oxidative stress.
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