Aconitine induces apoptosis in H9c2 cardiac cells via mitochondria-mediated pathway

Aconitine, a diterpenoid alkaloids derived from Aconitum plants, is widely employed to treat various diseases. The aim of the present study was to investigate the apoptotic effect of aconitine in H9c2 cardiac cells. H9c2 cell apoptosis induced by aconitine was detected by a Cell Counting kit-8 assay, DAPI staining, Annexin V-FITC/propidium iodide double staining and western blotting. The effects of aconitine on reactive oxygen species levels and mitochondrial membrane potential were confirmed by fluorescence microscopy and flow cytometry. In addition, ATP contents were determined using a ATP-dependent bioluminescence assay kit. The levels of peroxisome proliferator activated receptor γ co-activator 1α (PGC-1α) expression and apoptosis-associated proteins including Caspase-3, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and Cytochrome c were also assessed. Taken together, the results indicated that aconitine may inhibit cell viability, decrease PGC-1α expression, induce mitochondrial dysfunctions, upregulate Cytochrome c, Bax and Caspase-3, and downregulate Bcl-2, suggesting that aconitine may induce apoptosis through mitochondria-mediated signaling pathways in H9c2 cells.