Felodipine inhibits ox-LDL-induced reactive oxygen species production and inflammation in human umbilical vein endothelial cells.

Oxidative stress and inflammation are involved in the pathogenesis of atherosclerosis. Calcium channel blockers (CCBs) inhibit the development of atherosclerosis, although the underlying molecular basis has not been completely elucidated. The present study was designed to investigate the effects of felodipine, a CCB, on inflammation and oxidative stress in human umbilical vein endothelial cells (HUVECs) and to examine the underlying mechanisms of action. Oxidized low‑density lipoprotein (ox‑LDL) was used to induce an inflammatory response in HUVECs. The effects of felodipine were investigated by measuring the content of nitric oxide (NO) and reactive oxygen species (ROS), the mRNA and protein levels of intercellular adhesion molecule 1 (ICAM‑1) and vascular cell adhesion protein 1 (VCAM‑1), and the mRNA levels of endothelial NO synthase (eNOS) and inducible NO synthase (iNOS), in addition to the adhesion ability of U937 cells to HUVECs. ROS and NO levels were significantly increased in HUVECs following 24‑h treatment with 25 mg/l ox‑LDL (P<0.01). The increase in ROS was reversed by treatment with felodipine. In addition, NO levels were increased following treatment with 1 µmol/l felodipine (P<0.05). The mRNA expression of ICAM‑1, VCAM‑1, eNOS and iNOS was increased (P<0.05). Administration of 0.1 µM felodipine significantly decreased the expression of ICAM‑1, VCAM‑1, and iNOS (P<0.05). The number of U937 cells adhered to ox‑LDL‑treated HUVECs was significantly increased compared with control, which was reversed by felodipine (0.1 µM). In conclusion, felodipine was demonstrated to inhibit oxidative stress and inflammatory responses, suggesting that it may be used to treat atherosclerosis.