Different Effects of Testosterone to the Expression of Endothelial COX-2 in Normal and High Glucose Environment

Abstract

Male is one of the risk factors for the development of cardiovascular diseases. It is suggested that testosterone (T) may contribute to cardiovascular events, which is initiated by platelet adhesion, activation, and aggregation. Endothelial cells (EC) prevent platelet activation by synthesizing and releasing thromboregulator, such as prostacyclin (PGI2). The activity of cyclooxygenase (COX) enzyme is necessary for the conversion of arachidonic acid into PGI2. COX exists in two isomers: COX-1 and COX-2. This study aimed to examine the influence of T on the expression of endothelial COX-2 in either normal glucose (NG) or high glucose (HG) environment. An in vitro study using human umbilical vein endothelial cells culture (HUVEC) was performed in this study. With the 2x4 factorial designs, HUVEC was exposed to T in incremental doses: 0, 1, 10 and 10 2 nM in either NG (5.6 mM) or HG (22.4 mM) medium. Expression of COX-2 was measured using immunocytochemistry. Data were analyzed using analysis of variance for 2x4 factorial designs. P-value <0.05 was considered statistically significant. There was a main effect of either T or glucose medium to the percentage of EC that positively stained with the anti-COX-2 antibody. Moreover, there was an interaction between T and glucose medium to the percentage of EC that positively stained with the anti-COX-2 antibody. In conclusion, testosterone increases the expression of COX-2 enzyme in resting endothelial cells (normal glucose environment) but decreases significantly the expression of COX-2 enzyme in activated endothelial cells (high glucose environment).