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Sulforaphane prevents diabetes-induced liver ferroptosis through activation of Nrf2 signaling axis
dc.contributor | Conrad, Marcus | |
dc.contributor | Jiang, Xuejun | |
dc.contributor | Fedorova, Maria | |
dc.contributor | Friedmann Angeli, José Pedro | |
dc.creator | Otašević, Vesna | |
dc.creator | Grigorov, Ilijana | |
dc.creator | Savić, Nevena | |
dc.creator | Markelić, Milica | |
dc.creator | Veličković, Ksenija | |
dc.creator | Gudelj, Anđelija | |
dc.creator | Martinović, Vesna | |
dc.creator | Stančić, Ana | |
dc.date.accessioned | 2023-09-26T12:36:20Z | |
dc.date.available | 2900-01-01 | |
dc.date.issued | 2023 | |
dc.identifier.uri | http://radar.ibiss.bg.ac.rs/handle/123456789/6067 | |
dc.description.abstract | Recently, we characterized the ferroptotic phenotype of the liver of diabetic mice and revealed the inactivation of Nrf2 as an integral part of diabetes-induced liver ferroptosis. We aim here to examine does sulforaphane, an Nrf2 activator and antioxidant, prevent diabetes-induced liver ferroptosis and the mechanisms involved. For that purpose, male C57BL/6 mice were divided into three groups: control, diabetic (streptozotocin-treated, 40 mg/kg/5 consecutive days), diabetic+sulforaphane treated (2.5 mg/kg, from day 1-42). Results showed that diabetes-induced inactivation of Nrf2 and decreased expression of its downstream antiferroptotic parameters crucial for antioxidative defense (HO-1, catalase, SOD), iron metabolism (ferroportin, ferritin), glutathione synthesis (xCT, GCLC, CTH, CBS) and recycling (GR) were reversed/increased by sulforaphane treatment. Antiferroptotic effect of sulforaphane in the diabetic liver was further evidenced through the increased level of glutathione, decreased accumulation of liable iron and lipid peroxides (4-HNE) and decreased tissue damage (fibrosis and infiltration). Finally, diabetes-induced increase in serum glucose, ALT, AST and triglyceride level was significantly reduced by sulforaphane. These findings revealed for the first time that sulforaphane prevents in vivo diabetes-induced liver ferroptosis through activation of Nrf2 signaling axis. This suggests sulforaphane as a promising therapeutic tool for preventing ferroptosis at least in diabetes and diabetes-related pathologies. | sr |
dc.language.iso | en | sr |
dc.publisher | EMBO | sr |
dc.relation | 6525651‚Program saradnje srpske nauke sa dijasporom: Vaučeri za razmenu znanja, Fond za nauku Republike Srbije | sr |
dc.rights | restrictedAccess | sr |
dc.source | EMBO Workshop: Ferroptosis: When metabolism meets cell death; 2023 Apr 23-27; Seeon, Germany | sr |
dc.subject | diabetic mice | sr |
dc.subject | liver feroptosis | sr |
dc.subject | Nrf2 signaling | sr |
dc.subject | sulforaphane | sr |
dc.title | Sulforaphane prevents diabetes-induced liver ferroptosis through activation of Nrf2 signaling axis | sr |
dc.type | conferenceObject | sr |
dc.rights.license | ARR | sr |
dc.rights.holder | © 2023 by EMBO | sr |
dc.description.other | Conrad M, Jiang X, Fedorova M, Friedmann Angeli JP, editors. EMBO Workshop: Ferroptosis: When metabolism meets cell death; 2023 Apr 23-27; Seeon, Germany. EMBO; 2023. p. 39. | sr |
dc.citation.spage | 91 | |
dc.type.version | publishedVersion | sr |
dc.citation.rank | M34 | |
dc.identifier.rcub | https://hdl.handle.net/21.15107/rcub_ibiss_6067 |