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Endothelial dysfunction such as hyperpermeability is one of the characteristics in an early stage of diabetic complications. Curcumin has been shown to inhibit the formation of advanced glycation end products (AGEs) and to trap methyglyoxal (MGO) in cell-free system and in human umbilical vein endothelial cells (HUVECs). Here, we investigated the effect of curcumin on dysfunctions of HUVECs induced by exogenous MGO (30 μM), which significantly increased intracellular reactive oxygen species (ROS), endothelial permeability, and cytoskeleton rearrangement. In contrast, MGO decreased gap junctional intercellular communication and the expression of connexin 43 and zonula occludens. Pre-treatment of HUVECs with curcumin (0.25–2.5 μM) significantly ameliorated MGO-induced endothelial dysfunction, whereas pre-treatment with vitamin E (10 μM) only slightly ameliorated MGO-induced endothelial dysfunction, suggesting that ROS induced by MGO do not play a major role in endothelial dysfunction. These results suggest that curcumin is a potential protective agent against MGO-induced endothelial dysfunction.