Abstract:The effect of vomitoxin on the proliferation and apoptosis of human cardiomyocytes AC16 was explored in this study. After treatment of human cardiomyocytes AC16 with different concentrations of vomitoxin, the cell proliferation inhibition rate was detected by CCK-8 assay. The morphological changes of cells were observed by fluorescence microscopy, the cytotoxicity was detected by lactate dehydrogenase release, the shift in apoptosis rate was detected by Annexin V-FITC flow cytometric assay, and the change of mitochondrial membrane potential was detected by JC-1 fluorescent probe assay. The western blotting measured the apoptosis-associated proteins Bax and Bcl-2 expression levels. The results indicated that vomitoxin significantly inhibited cell proliferation and induced apoptosis in AC16 cells in a dose-dependent manner. Apoptosis rates of 14.89%, 43.20%, and 51.40% were observed after treatment with 2, 4, and 8 mol/L vomitoxin for 24 hours, respectively. The change in mitochondrial membrane potential expression level implied that vomitoxin may cause apoptosis of AC16 cells through the mitochondrial pathway. Western blotting results demonstrated up-regulation of Bax expression and down-regulation of Bcl-2 expression by vomitoxin. In summary, vomitoxin exerts a toxic effect on AC16 cells, significantly inhibiting cell growth and promoting cell death through apoptosis. The changes in mitochondrial membrane potential indicate that vomitoxin may induce the apoptosis of human cardiomyocytes AC16 through the mitochondrial pathway. The results provide theoretical support for further research on myocardial and cellular damage mechanisms by vomitoxin.
