Salidroside induces apoptosis via ERK1/2 in human leukemia K562 cells

Salidroside, a phenylpropanoid glycoside present in all species of Rhodiola genus, shows a broad spectrum of pharmacological properties. Here we investigated the effects of salidroside on the viability, cell cycle, apoptosis and its possible molecular mechanisms. Cell viability assay was used to evaluate the cytotoxic effects of salidroside on human leukemia K562 cells, and flow cytometry analyzed the change of cell cycle distribution, cell apoptosis, MMP level and ROS generation induced by salidroside. Western blotting further studied the expression changes of PCNA, CyclinD1, Bax, Bcl-2 and caspase-3, and the activation of ERK1/2 was also detected. We found that salidroside inhibited the growth of K562 cells in dose-and time-dependent manners, caused G2-M phase arrest and induced apoptosis via mitochondrial pathway. Salidroside could result in a decrease of PCNA, CyclinD1 and Bcl-2, and upregulated the levels of Bax and caspase-3 as well as inactivation of ERK1/2. In conclusion, these results suggest that salidroside inhibits cell viability and induces cell cycle arrest and apoptosis via inactivation of ERK1/2 signaling pathway in human leukemia K562 cells and may be a promising candidate for leukemia treatment.