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Cardiovascular diseases (CVD) are more frequently occurred in age-adjusted male subjects than female ones. It is suggested that testosterone (T) may contribute to the cardiovascular events, which is initiated by platelet adhesion, activation and aggregation. Endothelial cells (EC) prevent platelet activation and adhesion by synthesizing and releasing thromboregulator agents, including prostacycline (PGI2). Activity of cyclooxygenase (COX) enzyme is needed to catalyze conversion of arachidonic acid into prostaglandin, including PGI2. This study aimed to examine the influence of T to the expression of COX-2 in EC, in either resting (normal glucose environment) or stimulated (high glucose environment). We performed an in vitro experiment using human umbilical vein endothelial cells culture (HUVEC) with 2x4 factorial design. T was exposed to HUVEC in incremental doses: 0, 1, 10 and 102 nM in either normal glucose (5.6 mM) or high glucose (22.4 mM) concentration in treatment medium. Expression of COX-2 was measured using immunocytochemistry. Data were analyzed using independent t-test, one-way ANOVA and analysis of variance 2x4. P value <0.05 was considered significantly different. Percentage of EC positively stained with anti COX-2 antibody in NG medium without T was significantly lower than those with 1 nM, 10 nM and 102 nM T. Percentage of EC positively stained with anti COX-2 antibody in HG medium without T was significantly higher than those with 1 nM, 10 nM and 102 nM T. Exposure of T in incremental doses in either NG or HG medium significantly influenced percentage of EC positively stained with anti COX-2 antibody. There was main effect of glucose medium or T to percentage of EC positively stained with anti COX-2 antibody. Moreover, there was interaction between T and glucose medium to percentage of EC positively stained with anti COX-2 antibody. In conclusion, testosterone increases expression of COX-2 enzyme in resting endothelial cells (normal glucose environment) but decreases significantly expression of COX-2 enzyme in stimulated or activated endothelial cells (high glucose environment).