Effects of diazoxide on streptozotocin induced beta cell damage via HSP70/HSP90/TLR4/AMPK signaling pathways

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dc.contributor.authorKaya, Salih Tunç
dc.date.accessioned2023-07-26T11:50:06Z
dc.date.available2023-07-26T11:50:06Z
dc.date.issued2023
dc.departmentDÜ, Fen-Edebiyat Fakültesi, Biyoloji Bölümüen_US
dc.description.abstractI investigated the effects of diazoxide, a mitochondrial potassium channel opener, on streptozotocin (STZ) induced pancreatic beta cell damage via the HSP70/HSP90/TLR4/AMPK signaling pathways in vitro. I used the pancreatic beta cell line, 1.1B4, to create four groups: control, STZ treated, diazoxide treated, STZ + diazoxide treated. The STZ treated cells were exposed to 20 mu M STZ for 2 h with or without 100 mu M diazoxide for 24 h. Total antioxidant status (TAS), total oxidant status (TOS), cell viability and mitochondrial membrane potential (MMP) were measured. Expression of ATP-sensitive potassium channel (K-ATP) subunits, heat shock protein-70 (HSP70), heat shock protein-90 (HSP90), toll-like receptor 4 (TLR4), AMP-activated protein kinase (AMPK) and some apoptotic proteins were detected using western blotting. Apoptosis was assessed using TUNEL staining. STZ increased TOS and OSI in the pancreatic beta cells; however, diazoxide failed to improve oxidative stress. Also, STZ increased tunnel positive cells in the pancreatic beta cells. Diazoxide decreased the tunnel positive cells in the STZ treated beta cell. STZ decreased MMP; however, diazoxide did not normalize MMP in the STZ induced beta cells. Diazoxide increased the HSP70:HSP90 protein expression ratio. STZ decreased expression of AMPK and subunits of K-ATP channel and increased the expression of caspase-3 and TLR4 protein; diazoxide normalized the expression of all proteins studied. K-ATP channel opening by diazoxide protects pancreatic beta cells against STZ toxicity via HSP70/HSP90/TLR4/AMPK signaling.en_US
dc.identifier.doi10.1080/10520295.2023.2168757
dc.identifier.issn1052-0295
dc.identifier.issn1473-7760
dc.identifier.pmid36740984en_US
dc.identifier.scopus2-s2.0-85147652700en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1080/10520295.2023.2168757
dc.identifier.urihttps://hdl.handle.net/20.500.12684/12237
dc.identifier.wosWOS:000949206900001en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.institutionauthorKaya, Salih Tunç
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofBiotechnic & Histochemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmz$2023V1Guncelleme$en_US
dc.subjectAtp; Diabetes; Diazoxide; Hsp70; Hsp90; Human; Potassium Channel; Streptozotocinen_US
dc.subjectPancreatic-Islet; Atp; Protection; Mitochondria; Expression; Improves; Neurons; Stressen_US
dc.titleEffects of diazoxide on streptozotocin induced beta cell damage via HSP70/HSP90/TLR4/AMPK signaling pathwaysen_US
dc.typeArticleen_US

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