Taurine prevents high-glucose-induced human vascular endothelial cell apoptosis

Elevated blood glucose in uncontrolled diabetes is causally correlated with diabetic microangiopathy. Hyperglycemia-triggered accelerated endothelial cell apoptosis is a critical event in the process of diabetes-associated mi crovascular disease. The conditionally semiessential amino acid taurine has been previously shown to protect against human endothelial cell apoptosis. Therefore, this study was designed to investigate the role of taurine in t he prevention of high-glucose-mediated cell apoptosis in human umbilical ve in endothelial cells (HUVEC) and the mechanisms involved. Exposure of HUVEC to 30 mM glucose for 48 h (short-term) and 14 days (long-term) resulted in a significant increase in apoptosis, compared with normal glucose (5.5 mM; P < 0.05). High-glucose-induced DNA fragmentation preferentially occurred in the S phase cells. Mannitol (as osmotic control) at 30 mM failed to indu ce HUVEC apoptosis. Taurine prevented high-glucose-induced HUVEC apoptosis, which correlates with taurine attenuation of high-glucose-mediated increas ed intracellular reactive oxygen species (ROS) formation and elevated intra cellular Ca2+ concentration ([Ca2+](i)) level. Antioxidants, DMSO, N-acetyl cysteine, and glutathione, only partly attenuated high-glucose-induced HUV EC apoptosis. Glucose at 30 mM did not cause HUVEC necrosis. However, both glucose and mannitol at 60 mM caused HUVEC necrosis as represented by incre ased lactate dehydrogenase release and cell lysis. Taurine failed to preven t hyperosmolarity-induced cell necrosis. These results demonstrate that tau rine attenuates hyperglycemia-induced HUVEC apoptosis through ROS inhibitio n and [Ca2+](i) stabilization and suggest that taurine may exert a benefici al effect in preventing diabetes-associated microangiopathy.