Vitamin B6 protects vascular endothelial injury by activated platelets

Abstract

The protective effect of vitamin B6, in the form of pyridoxal-5-phosphate (PLP), on the function and integrity of vascular endothelium was investigated in cultured human umbilical vein endothelial cells (HUVECs) incubated with various concentrations of PLP. Prostacyclin (PGI 2) production from HUVECs assayed by radioimmunoassay (RIA) was used as an indicator of endothelial function. Endothelial integrity was determined by cell injury and cell turnover and survial rate. Endothdial injury was estimated by [H 3]-adenine release from HUVECs damaged by activated platelet (AP) or activated platelet lysate (APL). Turnover rates of HUVECs were defined by length of the time when 50% of confluent cells had detached from the monolayer. Survival rate was determined by the ratio of survival cell number to the total confluent cell number. Results showed that the production of PGI 2 was significantly higher when HUVECs were incubated with than without PLP. The addition of platelets, activated by collagen or lysed by sonication, to HUVECs resulted in time-dependent injury to the cells. Preincubation of HUVECs with PLP attenuated this cell injury. The optimal concentrations of PLP for cell against AP or APL injury were 1.0 and 1.5μM, respectively. Turnover and survival rates of HUVECs were delayed and increased, respectively, when HUVECs were incubated with increasing amounts of PLP from 0, 100, 200, 300 or 500 nM, although they were not significantly different. Data suggests that vitamin B6 protects endothelial cells by enhancing the beneficial function and preventing cell injury which are responsible for the initiation and the disease process of atherosclerosis.