Potent Ameliorative Effects of Rosmarinic Acid on Tramadol-Induced Neurotoxicity in the Brain and Hippocampus; by Suppressing Oxidative stress, Apoptosis, ER stress, and Regulating Cognitive Functions

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dc.authorid0000-0002-3339-4195
dc.contributor.authorKaraca, Onur
dc.contributor.authorŞimşek, Hasan
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorGür, Cihan
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorKandemir, Özge
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorKaraca, Şeyda Öte
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2025-07-17T10:27:20Z
dc.date.available2025-07-17T10:27:20Z
dc.date.issued2025
dc.departmentTıp Fakültesi
dc.description.abstractTramadol (TRM) is a synthetic opioid analgesic that acts on the central nervous system and is used to treat moderate or severe pain. However, the incidence of its abuse is increasing. Rosmarinic acid (RA) is a natural flavonoid known for its antioxidant, anti-inflammatory, and neuroprotective properties. In this study, we determined the ameliorative effects of RA against TRM-induced neurotoxicity. Thirty​​​​​​​ five rats were divided into 5 groups; control, RA, TRM, TRM + RA25 and TRM + RA50. TRM 50 mg/kg was administered intraperitoneally, and RA 25 and 50 mg/kg doses were administered by oral gavage for 14 days. Water Maze Test (WMT) was performed to assess cognitive function. Oxidative stress, inflammation, endoplasmic reticulum (ER) stress, apoptosis damage pathways, glial fibrillary acidic protein (GFAP), and brain-derived neurotrophic factor (BDNF) activities were determined in brain and hippocampus tissues. The structural and functional integrity of the tissues were also analyzed. RA decreased TRM-induced increased ​​​​​​​oxidative stress, inflammation, ER stress, and apoptotic damage levels. In addition, it improved neuronal survival and activity by bringing BDNF and GFAP activities closer to normal in brain tissue. RA restored the structural properties of brain and hippocampus tissues disrupted by tramadol. These findings were also demonstrated using WMT, which improved the arrival time to the quadrant in which the platform was located and the time spent in the quadrant. RA reduces TRM-induced neurotoxicity by reducing inflammation, oxidative stress, ER stress, and apoptotic damage and increases neuronal survival and activity.
dc.identifier.doi10.1007/s12035-025-04892-8
dc.identifier.issn08937648
dc.identifier.scopus105002164523
dc.identifier.urihttps://dx.doi.org/10.1007/s12035-025-04892-8
dc.identifier.urihttps://hdl.handle.net/20.500.12451/13350
dc.identifier.wosWOS:001461152300001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakScopus
dc.indekslendigikaynakWeb of Science
dc.institutionauthorKaraca, Onur
dc.institutionauthorŞimşek, Hasan
dc.institutionauthorAkaras, Nurhan
dc.institutionauthorKandemir, Özge
dc.institutionauthorKaraca, Şeyda Öte
dc.institutionauthorKndemir, Fatih Mehmet
dc.institutionauthorid0000-0002-3339-4195
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofMolecular Neurobiology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectApoptosis
dc.subjectCognitive Function
dc.subjectNeurotoxicity
dc.subjectOxidative Stress
dc.subjectRosmarinic Acid
dc.subjectTramadol
dc.titlePotent Ameliorative Effects of Rosmarinic Acid on Tramadol-Induced Neurotoxicity in the Brain and Hippocampus; by Suppressing Oxidative stress, Apoptosis, ER stress, and Regulating Cognitive Functions
dc.typeArticle

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