Figure 2.

Downregulation of miR-181a-5p alleviates CME-induced myocardial oxidative stress and inflammatory injury.

(A): Transfection with miR-181a-5p antagomiR decreased myocardial miR-181a-5p level significantly; (B & C): echocardiography was used to assess cardiac function and to quantify LVEF ( n = 10); (D & E): haematoxylin-basic fuchsin-picric acid staining was used to measure micro-infarction size (× 200 magnification, scale bar = 50 µm) ( n = 6); (F): serum cTnI concentration in each group (n = 10); (G & H): the ROS production was detected by the dichloro-dihydro-fluorescein diacetate assay (× 200 magnification, scale bar = 50 µm) ( n = 6); (I–L): myocardial MDA, SOD, GSH, and CAT level in each group (n = 6); and (M & N): western blotting was used to quantify myocardial TNF-α, IL-1β, and IL-6 protein level, with glyceraldehyde 3-phosphate dehydrogenase as a loading control ( n = 3). Data were shown as mean ± SE (standard error) based on at least three independent experiments. CAT: catalase enzymes; CME: coronary microembolization; cTnI: cardiac troponin I; GSH: glutathione; IL-1β: interleukin-1β; IL-6: interleukin 6; LVEF: left ventricular ejection fraction; MDA: malondialdehyde; ROS: reactive oxygen species; SOD: superoxide dismutase; TNF-α: tumor necrosis factor-α.