Fig 2: PPF treatment enhanced circAPBB2‐mediated effects in H/R‐treated AC16 cells. AC16 cells were divided into H/R group, H/R + OE‐circAPBB2 group, H/R + OE‐circAPBB2 group+150 μM of PPF group, with AC16 cells with normal treatment as controls. CircAPBB2 and miR‐18a‐5p expression were analyzed by qRT‐PCR (A, B) (N = 3). DUSP14 protein expression was analyzed by Western blot analysis assay (C) (N = 3). Cell viability was assessed by CCK‐8 assay (D) (N = 3). LDH, ROS and SOD levels were detected by commercial detection kits (E‐G) (N = 3). TNF‐α and IL‐1β levels were quantified by ELISAs (H, I) (N = 3). Cell apoptosis was quantified by flow cytometry assay (J) (N = 3). Cleaved caspase 3, cleaved PARP and Bcl‐2 expression were detected by Western blot analysis (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.

Fig 3: PPF treatment protected against H/R‐induced myocardial cell injury through miR‐18a‐5p. (A, B) The effects of PPF and H/R treatments on circAPBB2 and miR‐18a‐5p expression were analyzed by qRT‐PCR (N = 3). (C) The effects of PPF and H/R treatments on DUSP14 protein expression were analyzed by Western blot analysis assay (N = 3). AC16 cells were divided into H/R group, H/R + 150 μM PPF group, H/R + 150 μM PPF+miR‐18a‐5p group, with AC16 cells with normal treatment as controls. DUSP14 protein expression was analyzed by Western blot analysis assay (D) (N = 3). Cell viability was assessed by CCK‐8 assay (E) (N = 3). LDH, ROS and SOD levels were detected by commercial detection kits (F−G) (N = 3). TNF‐α and IL‐1β levels were quantified by ELISAs (I, J) (N = 3). Cell apoptosis was quantified by flow cytometry assay (K) (N = 3). Cleaved caspase 3, cleaved PARP and Bcl‐2 expression were detected by Western blot analysis (L) (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.

Fig 4: CircAPBB2 overexpression ameliorated H/R-induced myocardial cell injury by regulating miR-18a-5p. AC16 cells were divided into H/R group, H/R + OE-circAPBB2 group, H/R + OE-circAPBB2 group+miR-18a-5p 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-a and IL-1ß levels were quantified by ELISAs (F, G) (N = 3). Cell apoptosis was quantified by flow cytometry assay (H, 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-1ß, interleukin-1ß; LDH, Lactate dehydrogenase; ROS, reactive oxygen species; SOD, superoxide dismutase; TNF-a, tumor necrosis factor-a.