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目的探讨3-脱氧葡糖醛酮（3-DG）对人血管内皮细胞（VECs）存活的影响及作用机制。方法从人脐静脉分离血管内皮细胞并与不同浓度的3-DG在体外共同培养。细胞调亡用形态学和原位末端标记（TUNEL）法证实，凋亡或死亡细胞数量用FITCAnnexin-V及碘化丙碇（PI）染色后，以流式细胞仪检测。细胞内氧化水平以氧化敏感的荧光染料2，7-二氢二氯荧光素（DCFH）染色，用流式细胞仪测定。结果3-DG刺激后，内皮细胞出现凋亡的形态学变化且TUNEL阳性，调亡与死亡细胞数量随3-DG作用时间和浓度的增加而增多；同时，3－DG刺激后细胞内氧化水平升高；抗氧化剂N-乙酰半胱氨酸和羰基化合物清除剂氨基胍抑制3－DG引起的细胞氧化应缴并减少细胞凋亡与死亡。结论3－DG能够诱导VECs凋亡，其作用机制可能是通过增加细胞内氧化应激。这些结果提示糖尿病和慢性肾功能衰竭循环3－DG蓄积可能是这类患者血管并发症的发生机制之一。
Objective To investigate the effect of 3-deoxyglucosone (3-DG) on the survival of human vascular endothelial cells (VECs) and its mechanism. Methods Vascular endothelial cells were isolated from human umbilical vein and co-cultured with different concentrations of 3-DG in vitro. Cell apoptosis was confirmed by morphology and TUNEL method. The number of apoptotic or dead cells was detected by FITCAnnexin-V and propidium iodide (PI) staining and detected by flow cytometry. Intracellular oxidative levels were stained with the oxidation-sensitive fluorescent dye 2,7-dichlorodithluorofluorescein (DCFH) and determined by flow cytometry. Results After 3-DG stimulation, the morphological changes of apoptotic endothelial cells were observed and TUNEL was positive. The number of apoptotic and dead cells increased with the time and concentration of 3-DG. Meanwhile, the intracellular oxidative level Anti-oxidants N-acetylcysteine and carbonyl compound scavenger aminoguanidine inhibit 3-DG-induced cellular oxidative stress and reduce apoptosis and death. Conclusion 3-DG can induce apoptosis of VECs, and its mechanism may be through the increase of intracellular oxidative stress. These results suggest that circulating 3-DG accumulation in diabetes and chronic renal failure may be one of the mechanisms of vascular complications in these patients.