The role of CAPE in PI3K/AKT/mTOR activation and oxidative stress on testis torsion

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dc.contributor.authorDilber Y.
dc.contributor.authorInan S.
dc.contributor.authorErcan G.A.
dc.contributor.authorSencan A.
dc.date.accessioned2024-07-22T08:12:33Z
dc.date.available2024-07-22T08:12:33Z
dc.date.issued2016
dc.description.abstractIschemia reperfusion injury arises from testicular torsion resulting in a loss of spermatogenesis and significant germ cell apoptosis. This study evaluates the prooxidant/antioxidant effects of caffeic acid phenethyl ester (CAPE) through PI3K/AKT/mTOR signal pathways on testis torsion. A total of (28) male Wistar rats were divided randomly into 4 groups (n= 7 for each group):group A (sham) group,group B torsion/detorsion group, group C (saturation group, during four days of CAPE, one dose (10. μmol/kg, i.p)) and group D (a single dose of CAPE 2 h after torsion and before detorsion). At the end of the study, unilateral orchiectomies were performed for measurements of MDA and 8OHdG levels, histopathologic and immunohistochemical and TUNEL apoptotic cell examination. Testicular torsion-detorsion led to a significant decrease in the mean values of the Johnsen's scores and a significant increase in the apoptotic cell values of group B. There were no significant differences between group D and group A. In addition, the MDA and 8OHdG levels increased significantly in group B. The MDA and 8OHdG values were lower in group D. However, the 8OHdG levels were higher in group C than the groups A and D. On the other hand, CAPE suppresses mTOR activation and reduces the apoptosis on ischemia/reperfusion damage in rat testis. These results demonstrate that CAPE suppresses mTOR activation and reduces the apoptosis on ischemia/reperfusion damage in rat testis. © 2015 Elsevier GmbH.
dc.identifier.DOI-ID10.1016/j.acthis.2015.11.004
dc.identifier.issn00651281
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/16100
dc.language.isoEnglish
dc.publisherElsevier GmbH
dc.subjectAnimals
dc.subjectAntioxidants
dc.subjectCaffeic Acids
dc.subjectDrug Evaluation, Preclinical
dc.subjectMale
dc.subjectOxidative Stress
dc.subjectPhenylethyl Alcohol
dc.subjectPhosphatidylinositol 3-Kinases
dc.subjectProto-Oncogene Proteins c-akt
dc.subjectRats, Sprague-Dawley
dc.subjectSignal Transduction
dc.subjectSpermatic Cord Torsion
dc.subjectTestis
dc.subjectTOR Serine-Threonine Kinases
dc.subject8 hydroxydeoxyguanosine
dc.subjectcaffeic acid phenethyl ester
dc.subjectmalonaldehyde
dc.subjectmammalian target of rapamycin
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein kinase B
dc.subjectantioxidant
dc.subjectcaffeic acid derivative
dc.subjectcaffeic acid phenethyl ester
dc.subjectmTOR protein, rat
dc.subjectphenethyl alcohol
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein kinase B
dc.subjecttarget of rapamycin kinase
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectantioxidant activity
dc.subjectapoptosis
dc.subjectArticle
dc.subjectcontrolled study
dc.subjectenzyme activation
dc.subjecthistopathology
dc.subjectimmunohistochemistry
dc.subjectmale
dc.subjectnonhuman
dc.subjectorchiectomy
dc.subjectoxidative stress
dc.subjectprotein function
dc.subjectrat
dc.subjectreperfusion injury
dc.subjectsignal transduction
dc.subjectsingle drug dose
dc.subjecttestis detorsion
dc.subjecttestis detorsion
dc.subjecttestis disease
dc.subjecttestis torsion
dc.subjectTUNEL assay
dc.subjectanalogs and derivatives
dc.subjectanimal
dc.subjectdrug effects
dc.subjectmetabolism
dc.subjectpathology
dc.subjectpreclinical study
dc.subjectSprague Dawley rat
dc.subjecttestis
dc.subjecttestis torsion
dc.titleThe role of CAPE in PI3K/AKT/mTOR activation and oxidative stress on testis torsion
dc.typeArticle

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