Therapeutic potential of rosmarinic acid in tramadol-induced hepatorenal toxicity: Modulation of oxidative stress, inflammation, RAGE/NLRP3, ER stress, apoptosis, and tissue functions parameters

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dc.authorid0000-0002-3339-4195
dc.authorid0000-0001-6775-7858
dc.contributor.authorKaraca, Onur
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorŞimşek, Hasan
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorGencer, Selman
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2025-07-14T07:35:43Z
dc.date.available2025-07-14T07:35:43Z
dc.date.issued2025
dc.departmentTıp Fakültesi
dc.description.abstractTramadol (TRM), a widely used opioid analgesic for moderate to severe pain, is associated with liver and kidney toxicity at high doses or prolonged use. This study investigates the protective role of rosmarinic acid (RA), a natural phenolic compound known for its antioxidant, anti-inflammatory, and cell-protective properties, against TRM-induced hepatorenal toxicity. Methods: Thirty-five male Wistar rats were divided into five groups: Control, TRM, RA, TRM + RA25, and TRM + RA50. Rats received TRM (50 mg/kg) and RA (25 or 50 mg/kg), with liver and kidney function tests, oxidative stress, inflammation, ER stress, apoptosis, and tissue damage indicators assessed through qRT-PCR, ELISA, Western blotting, H&E, and immunohistochemical analysis. Results: TRM induced liver and kidney dysfunctions, evident from increased ALT, AST, ALP, urea, creatinine, nephrin, TIM-1 and 8-OHdG levels, along with activated oxidative stress, inflammation, ER stress, and apoptosis pathways. RA significantly reduced these effects, ameliorating histologic and immunohistochemical markers of tissue damage and inflammation. Conclusion: RA demonstrates therapeutic potential by mitigating TRM-induced hepatorenal toxicity and preserving tissue integrity.
dc.identifier.doi10.1016/j.fct.2025.115275
dc.identifier.issn02786915
dc.identifier.pmid39848458
dc.identifier.scopus85215995901
dc.identifier.urihttps://dx.doi.org/10.1016/j.fct.2025.115275
dc.identifier.urihttps://hdl.handle.net/20.500.12451/13285
dc.identifier.volume197
dc.identifier.wosWOS:001448306400012
dc.identifier.wosqualityQ2
dc.indekslendigikaynakPubMed
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorKaraca, Onur
dc.institutionauthorAkaras, Nurhan
dc.institutionauthorŞimşek, Hasan
dc.institutionauthorKandemir,, Fatih Mehmet
dc.institutionauthorid0000-0002-3339-4195
dc.language.isoen
dc.publisherElsevier Ltd
dc.relation.ispartofFood and Chemical Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectApoptosis
dc.subjectHepatorenal
dc.subjectOxidative Stress
dc.subjectRosmarinic Acid
dc.subjectToxicity
dc.subjectTramadol
dc.titleTherapeutic potential of rosmarinic acid in tramadol-induced hepatorenal toxicity: Modulation of oxidative stress, inflammation, RAGE/NLRP3, ER stress, apoptosis, and tissue functions parameters
dc.typeArticle

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