【摘要】目的 外源性硫化氢（H2S）对高糖诱导人腹膜间皮细胞损伤的保护作用及其可能的机制。方法 用4.25% D-葡萄糖（高糖）和5×10-5、10-4、5×10-4、10-3和5×10-3 mol/L的外源性H2S供体硫化氢钠(NaHS)处理人腹膜间皮细胞株HMrSV5细胞24 h，MTT比色法检测细胞活力，流式细胞术检测细胞内的内活性氧( ROS)水平，检测细胞内丙二醛（MDA）含量和超氧化物歧化酶（SOD）的活性。结果 与对照组比较，高糖组HMrSV5细胞活力显著降低，细胞培养液中LDH水平的显著增加，ROS水平显著增加，MDA含量显著增加而SOD的活性显著降低。与高糖组比较，5×10-4、10-3和5×10-3 mol/L的NaHS显著抑制了高糖诱导的HMrSV5细胞活力的降低和细胞培养液中LDH水平的增加。与高糖组比较，10-3 mol/L的NaHS显著抑制了高糖诱导的细胞内ROS和MDA水平的增加以及SOD活性降低。结论 外源性H2S抑制了高糖诱导的人腹膜间皮细胞损伤，其机制可能与外源性H2S抑制氧化应激有关。

【Abstract】Objective To investigate the protective effect of extrogenous hydrogen sulfide (H2S) on the injury of oxidative stress induced by high glucose in human peritoneal mesothelial cells line HMrSV5 cells. Methods HMrSV5 cells were incubated by 4.25% D-glucose (high glucose) to induce injury and cells were treated with a H2S donor sodium bisulfide (NaHS) for 24 h. MTT assay was used to detect the cell viability. The level of reactive oxygen species (ROS) was measured by flow cytometry. The level of lactate dehydrogenase (LDH) in the medium, The level of malondialdehyde (MDA) in the cells and the activity of superoxide dismutase (SOD) in the cells were measured. Results Compared with the control, the cell viability was singificantly decreased, the level of LDH in the medium was singificantly increased, the level of ROS in the cells was singificantly increased, the level of MDA in the cells was singificantly increased and the activity of SOD in the cells was singificantly decreased in high glucose group. Compared with the high glucose group, NaHS reversed the effect of high glucose. Conclusions Extrogenous H2S prevents the injury of oxidative stress induced by high glucose in human peritoneal mesothelial cells, which the mechanisms may be related to the inhibition of oxidative stress induced by H2S.