Salidroside prevents cadmium chloride-induced DNA damage in human fetal lung fibroblasts.

BACKGROUND

Cadmium (Cd) is an environmental pollutant and a heavy metal known for its genotoxic effects, which can lead to cancer and other related diseases. Preventing Cd-induced genotoxicity is crucial; however, there is limited research on this topic. Salidroside (SAL), a phenylpropanoid glycoside isolated from Rhodiola rosea L., is a popular medicinal compound with several health benefits. Nevertheless, its therapeutic effect on Cd-induced genotoxicity remains unexplored.

METHODS

Human fetal lung fibroblasts were treated with 20 μM Cd2+ (CdCl2) for 12 h and 5-20 μM SAL was used to test the anti-DNA damage effect. DNA damage was evaluated using γH2AX expression and the alkaline comet assay. Intracellular reactive oxygen species (ROS) levels were measured using flow cytometry.

RESULTS

Exposure to 20 μM Cd2+ for 12 h induced significant DNA damage in human fetal lung fibroblasts, and this effect was notably attenuated by SAL treatment. SAL treatment did not decrease ROS levels in cells treated with Cd2+.

CONCLUSION

SAL effectively prevented Cd2+-induced DNA damage in human fetal lung fibroblasts. However, the underlying mechanism requires further investigation.