Key result
Erythromycin, clarithromycin, and azithromycin significantly inhibited H9c2 cell growth and increased ERG1 gene expression in a concentration- and time-dependent manner, with azithromycin having the most pronounced effect.
Why the study?
Macrolides induce cardiotoxicity by blocking ERG potassium channels in cardiac myocytes, but their comparative effects on cell viability and ERG1 gene expression were unclear.
p-value: p=<0.05
Macrolide antibiotics, particularly azithromycin, demonstrate concentration- and time-dependent cytotoxicity and upregulation of ERG1 gene expression in H9c2 cardiomyoblasts, highlighting potential mechanisms for their known cardiotoxic effects.
Macrolides may promote cardiotoxicity via ERG1 in cardiomyocytes; animal data leaves open clinical relevance and needs human validation.
Background Macrolides are clinically well-established class of antibiotics. Macrolides induce cardiotoxicity by blocking ether-a-go-go–related gene (ERG) potassium channels in cardiac myocytes. The aim of this study was to compare the effects of erythromycin, clarithromycin and azithromycin on cell viability and expression of ERG1 gene in H9c2 cells. Methods Cell viability and ERG1 gene expression of H9c2 cells in 3 different concentrations, 1, 10 and 25µg/ml, after 48 and 72 hours were determined by MTT test and Real time-PCR method respectively. Results After 48 hours, the growth of H9c2 cells treated with erythromycin, clarithromycin and Azithromycin (except two doses) were inhibited significantly compared to control group (p <0.05). All three groups of antibiotics showed toxic effects on cells after 72 hours in all concentrations. Azithromycin-inhibiting effects were significantly higher than two other groups after 72 hours of treatment. The expression of ERG1 gene increased in all three groups of antibiotics by increasing the concentration and duration of treatment. Azithromycin had the most pronounced effect on ERG1 expression in 48 and 72 hours. Conclusions This study indicated that these macrolides affect ERG1 expression due to their potential cardiac adverse effects. Further investigations are required to understand the exact mechanism of cardiotoxicity associated with macrolides.
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Hajimirzaei et al. (2020) studied Cardiotoxicity. Erythromycin, clarithromycin, and azithromycin vs. Non-treated control was evaluated on Cell viability and ERG1 gene expression (p=<0.05). Erythromycin, clarithromycin, and azithromycin significantly inhibited H9c2 cell growth and increased ERG1 gene expression in a concentration- and time-dependent manner, with azithromycin having the most pronounced effect.
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