Objective To observe the production of hydrogen sulfide in endothelial cells exposed to high glucose as well as the effects of hydrogen sulfide on high glucose-induced injury of endothelial cells, and to explore the possible mechanisms. Methods Human umbilical vein endothelial cells were divided into 4 groups: A 5.5mmol/l glucose, B 25mmol/L glucose, C 25mmol/L glucose + 50μmol/L NaHS, and D 5.5mmol/L glucose+ 50μmol/L NaHS. After treatment for 48h, the production of H2S was measured, cell viability was detected by MTT, and the expressions of apoptosis-related proteins, such as Bax, Bcl-2 and cleaved caspase-3, were examined by Western Blot analysis. Results ① Compared with that of group A, the production of H2S distinctly decreased in group B(P<0.05), however, the production of H2S distinctly increased in group C when compared with that of group B(P<0.05). ② Compared with that of group A, the percentage of cell viability obviously decreased in group B (P<0.05), but NaHS could reverse the viability of HUVECs which was induced by high glucose in group C (P<0.05). ③ High glucose significantly increased Bax protein expression (P<0.05) and decreased the Bcl-2 protein expression (P<0.05), and the level of cleaved Caspase-3, the activated form of Caspase-3, was higher in group B compared with that of group A (P<0.05). Compared with that of group B, decrease in Bax (P<0.05) and cleaved Caspase-3 expressions (P<0.05) and increase in Bcl-2 expression (P<0.05) were observed in group C. There was no significant difference between group A and group D in cell viability, Bax, Bcl-2, cleaved Caspase-3 expressions and the production of H2S. Conclusions High glucose can inhibit the production of H2S in endothelial cells. Supplementation of extrinsic H2S can protect against high glucose-induced injury in human umbilical vein endothelial cells possibly through the inhibition of cell apoptosis.
