ArticleMolecular and cellular biochemistry2008
Caffeic acid phenethyl ester (CAPE) protects brain against oxidative stress and inflammation induced by diabetes in rats.
Article in Molecular and cellular biochemistry, 2008. 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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25 citing papers in PubMed, 92 citations in OpenAlex.
- Phenolic Compounds in Exercise Physiology: Dual Role in Oxidative Stress and Recovery Adaptation.Food science & nutrition · 2025Review
- Effects of Propolis Consumption on Liver Enzymes and Obesity Indices in Adults: A Systematic Review and Dose-Response Meta-Analysis.Current developments in nutrition · 2024Review
- Modulatory effect of caffeic acid in alleviating diabetes and associated complications.World journal of diabetes · 2023Review
- Oxidative Stress in Calcific Aortic Valve Stenosis: Protective Role of Natural Antioxidants.Antioxidants (Basel, Switzerland) · 2022Review
- CAPE and Neuroprotection: A Review.Biomolecules · 2021Review
- Caffeic Acid Phenethyl Ester Ameliorates Calcification by Inhibiting Activation of the AKT/NF-κB/NLRP3 Inflammasome Pathway in Human Aortic Valve Interstitial Cells.Frontiers in pharmacology · 2020Article
- Identification of Caffeic Acid Phenethyl Ester (CAPE) as a Potent Neurodifferentiating Natural Compound That Improves Cognitive and Physiological Functions in Animal Models of Neurodegenerative Diseases.Frontiers in aging neuroscience · 2020Article
- Protective Effects of Caffeic Acid Phenethyl Ester (CAPE) and Novel Cape Analogue as Inducers of Heme Oxygenase-1 in Streptozotocin-Induced Type 1 Diabetic Rats.International journal of molecular sciences · 2019Article
- Lixisenatide, a novel GLP-1 analog, protects against cerebral ischemia/reperfusion injury in diabetic rats.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Increased Indoleamine 2,3-Dioxygenase and Quinolinic Acid Expression in Microglia and Müller Cells of Diabetic Human and Rodent Retina.Investigative ophthalmology & visual science · 2017Article
- Neuroprotective Effect of Several Phytochemicals and Its Potential Application in the Prevention of Neurodegenerative Diseases.Geriatrics (Basel, Switzerland) · 2016Review
- Chronic type 2 diabetes reduces the integrity of the blood-brain barrier by reducing tight junction proteins in the hippocampus.The Journal of veterinary medical science · 2016Article
- Effect of sodium tungstate on visual evoked potentials in diabetic rats.International journal of ophthalmology · 2016Article
- Caffeic acid phenethyl ester inhibits liver fibrosis in rats.World journal of gastroenterology · 2015Article
- Treadmill exercise prevents diabetes-induced increases in lipid peroxidation and decreases in Cu,Zn-superoxide dismutase levels in the hippocampus of Zucker diabetic fatty rats.Journal of veterinary science · 2015Article
- Caffeic acid phenethyl amide ameliorates ischemia/reperfusion injury and cardiac dysfunction in streptozotocin-induced diabetic rats.Cardiovascular diabetology · 2014Article
- Aminoguanidine changes hippocampal expression of apoptosis-related genes, improves passive avoidance learning and memory in streptozotocin-induced diabetic rats.Cellular and molecular neurobiology · 2014Article
- Anti-neuroinflammatory effect of a novel caffeamide derivative, KS370G, in microglial cells.Molecular neurobiology · 2013Article
- Minocycline alleviates beta-amyloid protein and tau pathology via restraining neuroinflammation induced by diabetic metabolic disorder.Clinical interventions in aging · 2013Article
- Red orange: experimental models and epidemiological evidence of its benefits on human health.Oxidative medicine and cellular longevity · 2013Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic patients reveal significant disorders, such as nephropathy, cardiomyopathy, and neuropathy. As oxidative stress and inflammation seem to be implicated in the pathogenesis of diabetic brain, we aimed to investigate the effects of caffeic acid phenethyl ester (CAPE) on oxidative stress and inflammation in diabetic rat brain. Diabetes was induced by a single dose of streptozotocin (45 mg kg(-1), i.p.) injection into rats. Two days after streptozotocin treatment 10 microM kg(-1) day(-1) CAPE was administrated and continued for 60 days. Here, we demonstrate that CAPE significantly decreased the levels of nitric oxide and malondialdehyde induced by diabetes, and the activities of catalase, glutathione peroxidase, and xanthine oxidase in the brain. However, glutathione levels were increased by CAPE. The mRNA expressions of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma, and inducible nitric oxide synthase (iNOS) were remarkably enhanced in brain by diabetes. CAPE treatments significantly suppressed these inflammatory cytokines (about 70% for TNF-alpha, 26% for IFN-gamma) and NOS (completely). Anti-inflammatory cytokine IL-10 mRNA expression was not affected by either diabetes or CAPE treatments. In conclusion, diabetes induces oxidative stress and inflammation in the brain, and these may be contributory mechanisms involved in this disorder. CAPE treatment may reverse the diabetic-induced oxidative stress in rat brains. Moreover, CAPE reduces the mRNA expressions of TNF-alpha and IFN-gamma in diabetic brain; suggesting CAPE suppresses inflammation as well as oxidative stress occurred in the brain of diabetic patients.
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