Caffeic acid phenethyl ester (CAPE) protects brain against oxidative stress and inflammation induced by diabetes in rats

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dc.contributor.authorCelik, Sefa
dc.contributor.authorErdogan, Suat
dc.date.accessioned2024-09-18T20:15:09Z
dc.date.available2024-09-18T20:15:09Z
dc.date.issued2008
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractDiabetic 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 mu M 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.en_US
dc.identifier.doi10.1007/s11010-008-9719-3
dc.identifier.endpage46en_US
dc.identifier.issn0300-8177
dc.identifier.issn1573-4919
dc.identifier.issue1-2en_US
dc.identifier.pmid18265948en_US
dc.identifier.scopus2-s2.0-42149124840en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage39en_US
dc.identifier.urihttps://doi.org/10.1007/s11010-008-9719-3
dc.identifier.urihttps://hdl.handle.net/20.500.12483/9481
dc.identifier.volume312en_US
dc.identifier.wosWOS:000254905700006en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular and Cellular Biochemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectdiabetesen_US
dc.subjectcaffeic acid phenethyl esteren_US
dc.subjectoxidative stressen_US
dc.subjectinflammationen_US
dc.subjectbrainen_US
dc.subjectraten_US
dc.titleCaffeic acid phenethyl ester (CAPE) protects brain against oxidative stress and inflammation induced by diabetes in ratsen_US
dc.typeArticleen_US

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