Effects of alpha-tocopherol on ox-LDL-mediated degradation of IkappaB and apoptosis in cultured human coronary artery endothelial cells.

Experimental studies have demonstrated that vitamin E (alpha-tocopherol) may provide significant cytoprotection during cell injury. In this study, we examined the effects of alpha-tocopherol on oxidized low-density lipoprotein (ox-LDL)-induced apoptosis in human coronary artery endothelial cells (HCAECs). In addition, we examined the activation of NF-kappaB pathway in this process. Cultured HCAECs were treated with ox-LDL for 24 h. Incubation of HCAECs with ox-LDL resulted in apoptosis of HCAECs in a concentration-dependent manner, as determined by TUNEL and DNA laddering. Ox-LDL degraded IkappaB and activated NF-kappaB in HCAECs, as determined by Western blot analysis. Treatment with alpha-tocopherol (10 and 50 microM) decreased ox-LDL-mediated apoptosis as well as degradation of IkappaB and activation of NF-kappaB in HCAECs. High concentration of alpha-tocopherol (50 microM) was more effective than the low concentration of alpha-tocopherol (10 microM). Thus, ox-LDL induces apoptosis of HCAECs, in concurrence with degradation of IkappaB and activation of NF-kappaB. Alpha-tocopherol markedly decreases ox-LDL-induced effects.