Nevena Saksida
Cell death plays an important part in diabetes- convinced liver dysfunction. Ferroptosis is a recently defined regulated cell death caused by iron-dependent lipid peroxidation. Our former studies have shown that high glucose and streptozotocin( STZ) beget β- cell death through ferroptosis and that ferrostatin- 1 (Fer- 1), an asset of ferroptosis, improves β- cell viability, island morphology, and function. This study was aimed to examine in vivo the involvement of ferroptosis in diabetes- related pathological changes in the liver. For this purpose, manly C57BL/6 mice, in which diabetes was convinced with STZ (40 mg/kg/5 successive days), were treated with Fer- 1 (1 mg/kg, from day 1 – 21 day). It was set up that in diabetic mice Fer- 1 bettered serum situations of ALT and triglycerides and dropped liver fibrosis, hepatocytes size, and binucleation. This enhancement was due to the Fer-1-induced attenuation of ferroptotic events in the liver of diabetic mice, similar as accumulation of pro-oxidative parameters (iron, lipofuscin, 4-HNE), drop in expression position/ exertion of antioxidative defense- related motes (GPX4, Nrf2, xCT, GSH, GCL, HO-1, SOD), and HMGB1 translocation from nexus into cytosol. We concluded that ferroptosis contributes to diabetes- related pathological changes in the liver and that the targeting of ferroptosis represents a promising approach in the operation of diabetes- convinced liver injury.
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