Fig. 4

EGR2 overexpression deteriorates the hypoxia induced inflammation and apoptosis in cardiomyocytes. A The relative EGR2 mRNA expression level in cardiomyocytes induced by hypoxia indicated by qPCR, GAPDH was used as internal control, n = 3 in each group; B Western blot analysis of the relative EGR2 protein expression level in cardiomyocytes induced by hypoxia, GAPDH was served as internal control, n = 3 in each group; C Western blot analysis of EGR2 protein expression in cardiomyocytes with EGR2 gene overexpression mediated by lentiviral vector. GAPDH was served as internal contro; D the inflammation related genes expression in hypoxia-induced cardiomyocytes compared to normoxia-cultured cells detected by qPCR assays. GAPDH was served as internal control, n = 3 in each group; E qPCR analysis of the genes expression related to apoptosis in normoxia-cultured and hypoxia-induced cardiomyocytes. GAPDH was used as internal control, n = 3 in each group. F TUNEL staining show the apoptotic cells in hypoxia-induced cardiomyocytes, n = 3 in each group. *p < 0.05, **p < 0.01, n.s., no significant; All data are shown as the mean ± SD. Abbreviations: IL-6 interleukin 6, IL-1b interleukin 1b, CCL2 C–C motif chemokine ligand 2, TNF tumor necrosis factor, BAX BCL2 associated X, BAD BCL2 associated agonist of cell death, BCL2 B cell lymphoma protein-2