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Fig. 2 | Diabetology & Metabolic Syndrome

Fig. 2

From: Targeting ferroptosis with miR-144-3p to attenuate pancreatic β cells dysfunction via regulating USP22/SIRT1 in type 2 diabetes

Fig. 2

The effect of miR-144-3p on ferroptosis of INS-1 cells. The in vitro T2DM model was established by culturing INS-1 cells under high glucose (HG) condition. A The expression level of miR-144-3p in INS-1 cells after 24, 48, 72 h cultivation of HG was detected by RT-qPCR. B RT-qPCR detected the transfection efficiency of miR-144-3p inhibitor (left) and miR-144-3p mimic (right). C Under HG condition, the cell viability of INS-1 cells treating with or without miR-144-3p inhibitors or NC inhibitors; cell culturing under normal condition considered as negative control. D The cell viability of INS-1 cells treating with miR-144-3p mimics/inhibitors, erastin and Fer-1 (ferroptosis inducer and inhibitor) was detected by CCK-8 assay. E The cell viability of INS-1 cells treating with miR-144-3p mimics/inhibitors, staurosporine and ZVAD-FMK (apoptosis inducer and inhibitor). F The cell viability of INS-1 cells treating with miR-144-3p mimics, TNF-α and necrosulfonamide (necroptosis inducer and inhibitor). Under HG condition, INS-1 cells treating with Fer-1 or miR-144-3p mimics. G GSH content, H MDA levels, and I iron content of cells were measured using the corresponding detection kits. J Lipid ROS level was determined by the BODIPY™ 581/591 C11 method. K The levels of ferroptosis related proteins (GPX4 and TFR1) were evaluated by western blot. L Glucose stimulated insulin secretion was detected to assess β cells’ function (***P < 0.005 vs. INS-1 cells; ##P < 0.01 and ###P < 0.005 vs. HG-induced INS-1 cells)

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