南方医科大学学报2016，Vol.36Issue(8)：1055-1061,7.DOI:10.3969/j.issn.1673-4254.2016.08.05
外源性硫化氢通过调控瘦素/瘦素受体通路抑制高糖诱导的人脐静脉内皮细胞损伤
Exogenous hydrogen sulfide inhibits high-glucose-induced injuries via regulating leptin/leptin receptor signaling pathway in human umbilical vein endothelial cells
摘要
Abstract
Objective To investigate whether exogenous hydrogen sulfide (H2S) inhibits the high-glucose (HG)-induced injury by modulating leptin/leptin receptor (LEPR) signal pathway in human umbilical vein endothelial cells (HUVECs). Methods HUVECs were treated with 40 mmol/L glucose for 3-24 h, and the cell viability was examined by CCK-8 assay. The changes of cell morphology and the number of apoptotic cells were assessed by Hoechst 33258 nuclear staining followed by photofluorography. The intracellular levels of reactive oxygen species (ROS) was detected by DCFH-DA staining followed by photofluorography. Mitochondrial membrane potential (MMP) was determined by Rhodamine 123 (Rh123) staining and photofluorography. The expression levels of leptin and LEPR protein were measured by Western blotting. Results The expression of leptin and LERP in HUVECs began to significantly increase at 3 h after HG exposure and reached the peak levels at 9 h (P<0.01). Pretreatment of HUVECs with 400μmol/L sodium hydrosulfide (H2S donor) for 30 min inhibited HG-induced increase in leptin and leptin receptor expressions in HUVECs (P<0.01). Pretreatment of HUVECs with 400μmol/L NaHS for 30 min or 50 ng/mL leptin antagonists (LA) for 1 h obviously alleviated HG-induced injury by increasing cell viability, decreasing cell apoptosis and lowering accumulation of intracellular ROS and MMP loss (P<0.01). Conclusion Exogenous H2S protects against HG-induced injury by inhibiting leptin/LEPR pathway in HUVECs.关键词
硫化氢/瘦素/瘦素受体/高糖/人脐静脉内皮细胞Key words
hydrogen sulfide/leptin/leptin receptor/high glucose/human umbilical vein endothelial cells引用本文复制引用
吴冬波,陈景福,许庆,林佳琼,廖静秋,吴文..外源性硫化氢通过调控瘦素/瘦素受体通路抑制高糖诱导的人脐静脉内皮细胞损伤[J].南方医科大学学报,2016,36(8):1055-1061,7.基金项目
国家自然科学基金（81450062）；广东省自然科学基金（2015A030313872）Supported by National Natural Science Foundation of China (81450062) （81450062）
