Hesperidin has a protective effect on paclitaxel-induced testicular toxicity through regulating oxidative stress, apoptosis, inflammation and endoplasmic reticulum stress

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dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorKandemir, Özge
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorŞimsek, Hasan
dc.contributor.authorGenç, Aydın
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2023-10-03T07:11:12Z
dc.date.available2023-10-03T07:11:12Z
dc.date.issued2023
dc.departmentTeknik Bilimler Meslek Yüksekokulu
dc.description.abstractPaclitaxel (PTX) is widely used to treat a number of malignancies, although it has toxic side effects. Hesperidin (HES) has a wide range of biological and pharmacological properties, including anti-inflammatory and antioxidant abilities. This research aims to investigate the role of HES in PTX-induced testicular toxicity. For 5 days, 2 mg/kg/bw i.p. of PTX was administered to induce testicular toxicity. Rats were administered oral dosages of 100 and 200 mg/kg/bw HES for 10 days after PTX injection. The mechanisms of inflammation, apoptosis, endoplasmic reticulum (ER) stress, and oxidants were investigated using biochemical, genetic, and histological techniques. As a result of PTX administration, decreased antioxidant enzyme (superoxide dismutase, catalase, and glutathione peroxidase) activities and increased malondialdehyde level were regulated, and the severity of oxidative stress was reduced. NF-?B, IL-1? and TNF-? levels, which are among the increased inflammation parameters caused by PTX, decreased with HES administration. Although AKT2 gene expression decreased in PTX administered rats, it was determined that HES administration up-regulated AKT2 mRNA expression. Anti-apoptotic Bcl-2 decreased with PTX administration, and apoptotic Bax and Caspase-3 increased while HES administration reverted these effects towards control level. As a result of toxicity, the increase in ATF6, PERK, IRE1?, GRP78 levels caused prolonged ER stress, and this activity was diminished with HES and tended to regress. While all data were evaluated, Paclitaxel caused damage by increasing inflammation, apoptosis, ER stress and oxidant levels in testicular tissue, and Hesperidin showed a protective effect by correcting the deterioration in these levels.
dc.identifier.doi10.1016/j.reprotox.2023.108369
dc.identifier.issn0890-6238
dc.identifier.pmid36966900
dc.identifier.scopusqualityQ2
dc.identifier.urihttps:/dx.doi.org10.1016/j.reprotox.2023.108369
dc.identifier.urihttps://hdl.handle.net/20.500.12451/11048
dc.identifier.volume118en_US
dc.identifier.wosWOS:000967961700001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Inc.
dc.relation.ispartofReproductive Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectApoptosis
dc.subjectHesperidin
dc.subjectInflammation
dc.subjectOxidative Stress
dc.subjectPaclitaxel
dc.subjectTesticular Toxicity
dc.titleHesperidin has a protective effect on paclitaxel-induced testicular toxicity through regulating oxidative stress, apoptosis, inflammation and endoplasmic reticulum stress
dc.typeArticle

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