Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/6362
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
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