Fig 2: RUNX1/miR-142-3p/DRD2 pathway regulates the NF-κB-dependent inflammatory responses in H9c2 cells with H/R injury. (A) The NF-κB dependent inflammatory response was regulated by overexpression of RUNX1, miR-142-3p mimic and DRD2 in H9c2 cells with H/R injury and detected using western blotting. (B) Bar diagram showing the protein expression levels of RUNX1, DRD2, P65, TNF-α and IL-6 based on (A). n=3. (C) Bar diagram showing the protein expression of functional p-P65 subunit of NF-κB based on (A). n=3. *P<0.05, **P<0.01. H/R, hypoxia/reoxygenation; DRD2, dopamine receptor D2; p-, phosphorylated-; miR, microRNA; Ctrl, control.

Fig 3: miR-142-3p negatively regulates the expression of DRD2. (A) Reverse transcription-quantitative PCR for the identification of the downstream target gene of miR-142-3p by overexpressing miR-142-3p mimic in H9c2 cells. n=4. (B) The DRD2 protein levels were detected by western blotting in cardiac tissues with MIRI or miR-142-3p antagomir (anti-ago) treatment. (C) Summary for the protein expression of DRD2 based on (B), n=3. (D) DRD2 protein levels were detected by western blotting in H9c2 cells with H/R injury or emodin treatment. (E) Summary for the protein expression of DRD2 based on (D), n=3. (F) DRD2 protein levels were measured using western blotting in cardiac tissues with MIRI or emodin treatment. Three bands represent three independent samples. (G) Summary for the protein expression of DRD2 based on (F), n=3. *P<0.05, **P<0.01. NC, negative control; MIRI, myocardial ischemia/reperfusion injury; anti-ago, antagomir; DRD2, dopamine receptor D2; Ctrl, control; miR, microRNA; H/R, hypoxia/reoxygenation.