ArticleJournal of neurotrauma2012
Caffeic Acid phenethyl ester protects blood-brain barrier integrity and reduces contusion volume in rodent models of traumatic brain injury.
Article in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Preclinical progenitor cell therapy in traumatic brain injury: a meta-analysis.The Journal of surgical research · 2017Pooled it
- Alpha Lipoic Acid Mitigates TBI-Induced Neuroinflammation by Regulating S100B/STIM Signaling via NF-ƙB Pathway.Molecular neurobiology · 2026Article
- Blood-brain barrier breakdown in traumatic brain injury: current insights and future directions.Cancer gene therapy · 2026Review
- Much More than Nutrients: The Protective Effects of Nutraceuticals on the Blood-Brain Barrier in Diseases.Nutrients · 2025Review
- Caffeic Acid Phenethyl Ester Protects Neurons Against Oxidative Stress and Neurodegeneration During Traumatic Brain Injury.Biomolecules · 2025Article
- Caffeic acid phenethyl ester alleviates 1,2-dichloroethane-induced toxic cerebral edema: central and peripheral mechanisms.Frontiers in pharmacology · 2025Article
- Dietary (Poly)phenols in Traumatic Brain Injury.International journal of molecular sciences · 2023Review
- The neuroprotective potential of phytochemicals in traumatic brain injury: mechanistic insights and pharmacological implications.Frontiers in pharmacology · 2023Review
- Recent progresses in the pharmacological activities of caffeic acid phenethyl ester.Naunyn-Schmiedeberg's archives of pharmacology · 2021Review
- CAPE and Neuroprotection: A Review.Biomolecules · 2021Review
- Insulin-Like Growth Factor-2 (IGF-2) Does Not Improve Memory in the Chronic Stage of Traumatic Brain Injury in Rodents.Neurotrauma reports · 2021Article
- Neuroprotective Potential of Caffeic Acid Phenethyl Ester (CAPE) in CNS Disorders: Mechanistic and Therapeutic Insights.Current neuropharmacology · 2021Article
- Combined treatment with GSNO and CAPE accelerates functional recovery via additive antioxidant activities in a mouse model of TBI.Journal of neuroscience research · 2018Article
- Neuroprotective Effect of Caffeic Acid Phenethyl Ester in A Mouse Model of Alzheimer's Disease Involves Nrf2/HO-1 Pathway.Aging and disease · 2018Article
- iTRAQ-Based Quantitative Proteomics Reveals the New Evidence Base for Traumatic Brain Injury Treated with Targeted Temperature Management.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Article
- Caffeic acid phenethyl ester attenuates neuropathic pain by suppressing the p38/NF-κB signal pathway in microglia.Journal of pain research · 2018Article
- Review
- Natural Compounds as a Therapeutic Intervention following Traumatic Brain Injury: The Role of Phytochemicals.Journal of neurotrauma · 2017Review
- Acid fibroblast growth factor preserves blood-brain barrier integrity by activating the PI3K-Akt-Rac1 pathway and inhibiting RhoA following traumatic brain injury.American journal of translational research · 2017Article
- Cognitive assessment of pycnogenol therapy following traumatic brain injury.Neuroscience letters · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
A number of studies have established a deleterious role for inflammatory molecules and reactive oxygen species (ROS) in the pathology of traumatic brain injury (TBI). Caffeic acid phenethyl ester (CAPE) has been shown to exert both antioxidant and anti-inflammatory effects. The primary objective of the present study was to examine if CAPE could be used to reduce some of the pathological consequences of TBI using rodent models. Male Sprague-Dawley rats and C57BL/6 mice were subjected to controlled cortical impact (CCI) injury. Blood-brain barrier (BBB) integrity was assessed by examining claudin-5 expression and the extravasation of Evans blue dye. The effect of post-injury CAPE administration on neurobehavioral function was assessed using vestibulomotor, motor, and two hippocampus-dependent learning and memory tasks. We report that post-TBI administration of CAPE reduces Evans blue extravasation both in rats and mice. This improvement was associated with preservation of the levels of the tight junction protein claudin-5. CAPE treatment did not improve performance in either vestibulomotor/motor function (tested using beam balance and foot-fault tests), or in learning and memory function (tested using the Morris water maze and associative fear memory tasks). However, animals treated with CAPE were found to have significantly less cortical tissue loss than vehicle-treated controls. These findings suggest that CAPE may provide benefit in the treatment of vascular compromise following central nervous system injury.
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Registered trials
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.