Amiodarone promotes heat-induced apoptosis, inflammation and oxidative stress in mouse HL1 atrial myocytes

Abstract

To investigate the injury types of atrial myocytes induced by heat exposure and the effect of amiodarone on heat-induced injuries in atrial myocytes. The optimal temperature for heat exposure and optimal concentration of amiodarone were determined by measuring the cell viability exposed to different temperatures and different concentrations of amiodarone. Heat exposure of HL1 atrial myocytes was conducted using a water bath, and the effect of amiodarone on cell viability was assessed with MTS method; cell apoptosis was detected using flow cytometry, and the levels of IL-1β, IL-6, TNF-α, SOD and MDA were detected with enzyme-linked immunosorbent assay (ELISA). Compared with the blank control cells, the cells exposed to a temperature of 52 ℃ showed a significantly decreased survival rate and a lowered SOD activity (P < 0.001) with increased IL-1β and MDA levels (P < 0.01) and markedly increased apoptosis rate and IL-6 level (P < 0.001). Compared with the heat exposure group, amiodarone resulted in significantly decreased survival rate of the atrial myocytes (P < 0.01), obviously decreased SOD activity (P < 0.05), and increased cell apoptosis rate (P < 0.05) and IL-1β, IL-6, MDA and TNF-α levels (P < 0.01 or 0.001). Heat exposure induces apoptosis, inflammation and oxidative stress in mouse HL1 atrial myocytes, and amiodarone can enhance the effects of heat exposure to aggravate the cell injuries.