Fig 1: MiR‐18a‐5p depletion ameliorated H/R‐induced myocardial cell injury by regulating DUSP14. AC16 cells were divided into H/R group, H/R+anti‐miR‐18a‐5p group, H/R+anti‐miR‐18a‐5p+si‐DUSP14 group, with AC16 cells with normal treatment as controls. DUSP14 protein expression was analyzed by Western blot analysis assay (A) (N = 3). Cell viability was assessed by CCK‐8 assay (B) (N = 3). LDH, ROS, and SOD levels were detected by commercial detection kits (C‐E) (N = 3). TNF‐α and IL‐1β levels were quantified by ELISAs (F and G) (N = 3). Cell apoptosis was quantified by flow cytometry assay (H and I) (N = 3). Cleaved caspase 3, cleaved PARP and Bcl‐2 expression were detected by Western blot analysis (J, K) (N = 3). *p < .05, **p < .01 and ***p < .001. Significant differences were determined using one‐way analysis of variance with Tukey's test. Bcl‐2, B‐cell lymphoma‐2; CCK‐8, cell counting kit‐8; H/R, hypoxia/reoxygenation; IL‐1β, interleukin‐1β; LDH, Lactate dehydrogenase; ROS, reactive oxygen species; SOD, superoxide dismutase; TNF‐α, tumor necrosis factor‐α.