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

Figure 2 Treatment with Farrerol alleviated cardiac microvascular injury in diabetic cardiomyopathy mice. A and B: Cardiac microvascular density was determined using CD31-positive endothelial cells (ECs), and large vessels were excluded (n = 6 per fields); C: Perivascular leakage of albumin was detected by immunofluorescence staining and quantified. Bar = 50 μm; D-F: Protein expression of intercellular adhesion molecule-1 and endothelial nitric oxide synthase (eNOS) were detected by western blot and quantified (n = 3); G: Representative immunofluorescence images of endothelial anchoring junctions (VE-cadherin). Bar = 100 μm; H: In vitro endothelial monolayer permeability was determined based on FITC-BSA leakage (n = 6 per group); I and J: Representative images of immunofluorescence staining of Intercellular adhesion molecule-1 (VCAM-1) and quantitative analysis of VCAM-1 intensity. Bar = 20 μm. n = 6 per fields; K-M: Immunoblots and quantitative data of VCAM-1 and eNOS expression in high glucose and free fatty acid treated ECs (n = 3). ^aP < 0.05 vs NC; ^bP < 0.05 vs DCM or HG/FFA. FA: Farrerol; DCM: Diabetic cardiomyopathy; HG/FFA: High glucose and free fatty acid.