Triclosan stimulates human vascular endothelial cell injury via repression of the PI3K/Akt/mTOR axis.

Triclosan (TCS) has potentially toxic effects on humans and animals. However, the possible roles and mechanisms of TCS in endothelial cells (ECs) are still unknown. Abnormal damage to ECs and vascular function is a critical process in various cardiovascular diseases, including coronary artery disease (CAD), atherosclerosis, stroke, and hypertension. Hence, we explored the potential toxicological roles of TCS in EC functions. Cell Counting Kit-8, apoptosis, transwell, wound healing, and tube-formation experiments were performed to evaluate the effects of TCS on human umbilical vein endothelial cell (HUVEC) function. Additionally, the levels of PI3K, Akt, and mTOR phosphorylation were measured by Western blot. The results indicated that TCS treatment suppressed HUVECs viability, migration and angiogenesis. TCS treatment increased the expression of inflammatory markers and ROS in cultured HUVECs. Moreover, TCS treatment inhibited PI3K/Akt/mTOR expression. All of these results reveal that TCS induces notable vascular injury and affects the viability, migration and angiogenic capacity of HUVECs, at least in part via the PI3K/Akt/mTOR signaling pathway.