Farrerol ameliorates diabetic cardiomyopathy by inhibiting ferroptosis via miR-29b-3p/SIRT1 signaling pathway in endothelial cells

Figure 10  SIRT1 was involved in the protective effects of Farrerol and miR-29b-3p on high glucose and free fatty acid-induced endothelial cells dysfunction. A: Knockdown of SIRT1 was achieved by transfected siRNA into Human umbilical vein Endothelial cells and confirmed by western blot analysis (n = 3); B: Cell viability was detected via cell counting kit-8 (CCK-8) assay in endothelial cells (ECs) after indicated treatments (n = 6); C-E: Western blots analysis and quantitative data of GPX4 and xCT expression in high glucose and free fatty acid (HG/FFA) treated ECs (n = 3); F: Representative immunofluorescence images of the intensity endothelial anchoring junctions (VE-cadherin). Bar = 100 μm; G: In vitro endothelial monolayer permeability was determined based on FITC-BSA leakage (n = 6 per group); H: Cell viability was detected via CCK-8 assay in ECs with SIRT silencing (n = 6); I-K: Western blots analysis and quantitative data of GPX4 and xCT expression in HG/FFA treated ECs (n = 3); L: Representative immunofluorescence images of the intensity endothelial anchoring junctions (VE-cadherin). Bar = 100 μm; M: In vitro endothelial monolayer permeability was determined based on FITC-BSA leakage (n = 6 per group). ^aP < 0.05 vs NC; ^bP < 0.05 vs HG/FFA; ^cP < 0.05 vs HG/FFA + miR-29b-3p mimic. HG/FFA: High glucose and free fatty acid.