The role of toll-like receptors in the protective effect of melatonin against doxorubicin-induced pancreatic beta cell toxicity

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dc.contributor.authorTaşkın, Eylem
dc.contributor.authorGüven, Celal
dc.contributor.authorKaya, Salih Tunç
dc.contributor.authorŞahin, Leyla
dc.contributor.authorKocahan, Sayad
dc.contributor.authorDeğirmencioğlu, Arife Zuhal
dc.contributor.authorSevgiler, Yusuf
dc.date.accessioned2020-04-30T23:34:30Z
dc.date.available2020-04-30T23:34:30Z
dc.date.issued2019
dc.departmentDÜ, Fen-Edebiyat Fakültesi, Biyoloji Bölümüen_US
dc.descriptionSevgiler, Yusuf/0000-0002-4373-2389en_US
dc.descriptionWOS: 000484035300029en_US
dc.descriptionPubMed: 31369761en_US
dc.description.abstractAims: Doxorubicin, an anticancer drug, has a toxic effect on many tissues such as heart, pancreas, liver, kidney, and testis. The aim of current study is to investigate whether melatonin would be protective in doxorubicin-induced beta (beta) cell toxicity via HMGB1/TLR2/TLR4/MAPK/NF-kappa B signaling pathway. Main methods: Human pancreatic beta cell (1.1B4) was used in the present study. Four experimental groups were created as control, melatonin (10 mu M), doxorubicin (2 mu M) and the combination of melatonin with doxorubicin. Following 24-h treatment, Mitogen-activated protein kinase (MAPKs), Toll like receptors (TLRs) including TLR2 and TLR4, pro-and anti-apoptotic protein expression levels were determined by western blotting. Total antioxidant (TAS), oxidant status (TOS) and oxidative stress index (OSI) of the cells as well as superoxide dismutase (SOD) levels were determined. Active caspase-8 activity was measured and TUNEL staining was performed to study apoptotic pathways. Mitochondrial membrane potential (MMP), some protein expressions and F-actin distribution were analyzed. Key findings: Doxorubicin caused to depolarize MMP, resulting in enhancing apoptosis by activation of caspase-8 via MAPKs/NF-kappa B pathway via elevation of TOS and decreasing TAS. Also, doxorubicin destroyed F-actin distribution and elevated TLR2 and some apoptotic proteins, including Bax. However, co-treatment of melatonin with doxorubicin could reverse depolarization of MMP and inhibition of apoptosis through MAPK/NF-kappa B signaling by decreasing TOS and increasing TAS. The co-treatment reversed the alternations of TLR2, TLR4, MAPKs and apoptotic protein expressions induced by doxorubicin. Significance: Melatonin could be a good candidate against pancreatic beta cell toxicity-induced by doxorubicin through TLR2/TLR4/MAPK/NF-kappa B pathways.en_US
dc.description.sponsorshipNigde Omer Halisdemir University Scientific Research Projects Coordination Unit, Nigde/Turkey [SSB2017/01-BAGEP]en_US
dc.description.sponsorshipThis work was supported by the Nigde Omer Halisdemir University Scientific Research Projects Coordination Unit, Nigde/Turkey [grant number SSB2017/01-BAGEP]en_US
dc.identifier.doi10.1016/j.lfs.2019.116704en_US
dc.identifier.issn0024-3205
dc.identifier.issn1879-0631
dc.identifier.scopusqualityQ1en_US
dc.identifier.urihttps://doi.org/10.1016/j.lfs.2019.116704
dc.identifier.urihttps://hdl.handle.net/20.500.12684/5175
dc.identifier.volume233en_US
dc.identifier.wosWOS:000484035300029en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherPergamon-Elsevier Science Ltden_US
dc.relation.ispartofLife Sciencesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectDoxorubicinen_US
dc.subjectMelatoninen_US
dc.subjectBeta cellen_US
dc.subjectToll like receptorsen_US
dc.subjectOxidative stressen_US
dc.subjectProtein kinasesen_US
dc.titleThe role of toll-like receptors in the protective effect of melatonin against doxorubicin-induced pancreatic beta cell toxicityen_US
dc.typeArticleen_US

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