Abstract

AbstractThe objective of this study was to elucidate the different mechanisms of low‐density lipoprotein (LDL) oxidation by human endothelial cells. High level of LDL stimulated human alpha‐defensin 1 (HNP‐1) expression strongly, activated myeloperoxidase (MPO), and accumulated malondialdehyde (MDA). In addition, lipopolysaccharides (LPS) had similar effect, however the cell response occurred even earlier. After 12 h of LDL co‐culture, the cells were washed and fresh LDL was added again. MPO activity and MDA generation were increased. Adding fresh LDL after the LPS co‐culture for 3 h, a similar trend, however weaker effect was observed. Culturing cells with LDL and adding various kinds of calcium antagonists at the same time did not make obvious changes to the expression of HNP‐1. In contrast, culturing cells with LPS, calcium antagonists increased HNP‐1 expression. Adding the anti‐radical drug sodium ferulate had no significant effect on oxidative function activated by LDL, but the oxidation activated by LPS was suppressed significantly and the HNP‐1 expression was not changed significantly. The endogenous irritant LDL and the exogenous irritant LPS activated human endothelial cells in different manners and HNP‐1 expression changes were involved.

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