Induction of apoptosis in acute myeloid leukemia HL-60 cells by bufotalin via mitochondrial pathway

Objective To study the effect of bufotalin on acute myeloid leukemia HL-60 cells and its mechanism, so as to provide new ideas for the treatment of acute myeloid leukemia. Methods The HL-60 cells in the logarithmic growth phase were treated with quercetin at a final concentration of 0, 40, 80, and 160 μg/mL for 24 h, and the cell proliferation was detected by CCK-8 kit. The mitochondrial morphology was observed by transmission electron microscopy. The expressions of Bax, Bcl-2 and Cleaved-Caspase-9 genes were detected by Western blotting. The toxic effects of the compounds on normal cells were observed by using normal peripheral blood B lymphocytes as control group. The results of the experiment were recorded with SPSS 22.0 and tested. P<0.05 was considered statistically significant. Results Bufotalin could inhibit the proliferation of HL-60 cells and induce its apoptosis, and its normal cytotoxicity is smaller than that of cancer cells, with statistical significance (P<0.05). With the increase of drug concentration, nuclear showed abnormalities, nuclear membrane showed separation, and heterochromatin increased significantly, along with mitochondria with edema expansion, fuzzy disappearance of some mitochondrial ridges and vacuolization, while the control mitochondria morphology was better. When the proportion of Bax/Bcl-2 increased, Cleaved-Caspase-9 gene expression increased gradually, and the difference was statistically significant (all P<0.01). Conclusion The results of this experiment indicate that bufotalin also inhibits non-solid tumor cells of acute myeloid leukemia HL-60 cells, and has less impact on normal cells. The mechanism of its action is mainly to induce tumor cell apoptosis through mitochondrial pathway.