[ERK1/2 mediates edaravone-triggered protection against myocardial damage induced by isoprenaline in H9c2 cells].

Objective To explore the effect of extracellular signal regulated kinase 1/2 (ERK1/2) on edaravone (EDA) -triggered protection against myocardial toxicity induced by isoprenaline (ISO) in H9c2 myocardial cells (H9c2 cells). Methods H9c2 cells were exposed to ISO at different concentrations to establish a cardiac toxicity model induced by persistent excitation of β1 receptor. EDA was added before ISO as a pretreatment. PD-98059,an ERK1/2 inhibitor,was administered 1 h prior to EDA to inhibit the phosphorylation of ERK1/2. Cell viability was measured using cell counter kit (CCK-8). The expressions of p-ERK1/2 and t-ERK1/2 were tested by Western blotting. Mitochondrial membrane potential (MMP) was detected by Rhodamine123 (Rh123) staining and photofluorography. Results Exposure of H9c2 cells to 80 μmol/L ISO for 24 h down-regulated ERK1/2 phosphorylation and repressed MMP. Pretreatment with 10-40 μmol/L EDA for 1 h inhibited ISO-induced myocardial toxicity and pretreatment of 40 μmol/L EDA partially rescued ERK1/2 phosphorylation and MMP level. PD-98059 abolished cardiac protection of EDA,leading to myocardial toxicity and MMP loss. Conclusion EDA can protect H9c2 cells against myocardial injury induced by ISO by suppressing ISO-triggered inhibition of ERK1/2 activation.