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Title: | Sulforaphane prevents diabetes-induced liver ferroptosis through activation of Nrf2 signaling axis | Authors: | Vesna Otašević Ilijana Grigorov Nevena Savić Markelić, Milica Veličković, Ksenija Anđelija Gudelj Vesna Martinović Ana Stančić |
Keywords: | Sulforaphane;ferroptosis;Nrf2;diabetes | Issue Date: | 23-Apr-2023 | Rank: | M34 | Publisher: | EMBO | metadata.dc.identifier.artno: | 039 | Start page: | 91 | Conference: | EMBO Workshop "Ferroptosis: When metabolism meets cell death" | 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. |
URI: | https://biore.bio.bg.ac.rs/handle/123456789/6362 |
Appears in Collections: | Conference abstract |
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