Docetaxel-induced liver and kidney toxicity in rats can be alleviated by suppressing oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis and autophagy signaling pathways after Silymarin treatment

dc.authorid0000-0001-8884-4168
dc.authorid0000-0002-8222-5515
dc.authorid0000-0001-6775-7858
dc.contributor.authorKandemir, Özge
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorÇomaklı, Selim
dc.contributor.authorGür, Cihan
dc.contributor.authorİleritürk, Mustafa
dc.date.accessioned2025-04-15T06:18:50Z
dc.date.available2025-04-15T06:18:50Z
dc.date.issued2025
dc.departmentGüzelyurt Meslek Yüksekokulu
dc.description.abstractApproximately 20 million new cancer cases have occurred worldwide, and dose limitation occurs because of the liver and kidney toxicity of chemotherapeutic agents. Inflammation/apoptosis/ROS pathways appear to be activated in the liver and kidney toxicity of chemotherapeutic agents. This study was conducted to investigate the potential effects of silymarin (SLY) use against docetaxel (DTX)-induced liver and kidney damage in rats. For this purpose, 30 mg/kg DTX was administered intraperitoneally to Sprague Dawley rats on the first day of the study, followed by SLY (25 or 50 mg/kg/day) orally for 7 days. Then, various analyses were performed on liver and kidney tissues using biochemical, molecular and histological methods. The data obtained showed that DTX administration suppressed antioxidant markers and increased lipid peroxidation in liver and kidney tissues. It was also determined that DTX administration triggered markers of endoplasmic reticulum stress, inflammation, apoptosis and autophagy. On the other hand, SLY treatment increased enzymatic and non-enzymatic antioxidant levels and decreased malondialdehyde levels. Additionally, SLY alleviated DTX-induced endoplasmic reticulum stress, inflammation, apoptosis and autophagy in liver and kidney tissues. Immunohistochemical analyses showed that DTX increased the density of 8-OHdG positive cells in liver and kidney tissues, while oxidative DNA damage decreased after SLY administration. ALT, AST, ALP, Urea and Creatinine levels increased in the DTX group and decreased in the SLY treatment groups. In conclusion, DTX administration caused toxicity in liver and kidney tissues and damaged tissue integrity, while SLY treatment alleviated DTX-induced toxicity.
dc.identifier.doi10.1016/j.fct.2024.115202
dc.identifier.issn0278-6915 / 1873-6351
dc.identifier.scopus2-s2.0-85212557892
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://dx.doi.org/10.1016/j.fct.2024.115202
dc.identifier.urihttps://hdl.handle.net/20.500.12451/13038
dc.identifier.volume196
dc.identifier.wos001393960000001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.institutionauthorKandemir, Özge
dc.institutionauthorid0000-0001-8884-4168
dc.language.isoen
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofFood and Chemical Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectDocetaxel
dc.subjectEndoplasmic Reticulum Stress
dc.subjectHepatorenal Toxicity
dc.subjectOxidative Stress
dc.subjectPreclinical Test
dc.subjectSilymarin
dc.titleDocetaxel-induced liver and kidney toxicity in rats can be alleviated by suppressing oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis and autophagy signaling pathways after Silymarin treatment
dc.typeArticle

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