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目的:观察糖基化终末产物(AGEs)对人腹膜间皮细胞(HPMC)分泌血管内皮生长因子(VEGF)的影响及细胞内活性氧(ROS)在其中的作用。方法:分别用不同浓度的AGE-HSA及抗氧化剂N-酰-L-半胱氨酸(NAC)作用于细胞,用RT-PCR和ELISA方法测定HPMC中VEGF的表达;再以氧化敏感的荧光染料2、7-二氢二氯荧光素(DCFH)染色,流式细胞仪测定细胞内活性氧强度。结果:AGE-HSA能使细胞内ROS水平明显升高,呈现浓度依赖效应;AGE-HSA同时以时效和量效方式促进HPMC中VEGF的表达;而NAC能够明显抑制AGE-HSA所导致的细胞内ROS升高,同时抑制HPMC中VEGF的分泌。结论:AGE-HSA可能部分通过诱导细胞内ROS,促进HPMC表达VEGF,从而引起腹膜新生血管的增加,最终导致腹膜失超滤现象。
Objective: To investigate the effects of advanced glycation end products (AGEs) on the secretion of vascular endothelial growth factor (VEGF) from human peritoneal mesothelial cells (HPMC) and the role of intracellular reactive oxygen species (ROS) in them. Methods: AGE-HSA with different concentrations of N-acyl-L-cysteine (NAC) were used in cells respectively. The expression of VEGF in HPMC was determined by RT-PCR and ELISA. Dye 2, 7-dichlorodifluorescein (DCFH) staining, flow cytometry determination of intracellular reactive oxygen species. Results: AGE-HSA significantly increased intracellular ROS levels in a concentration-dependent manner. AGE-HSA promoted the expression of VEGF in HPMC both in a time and dose-dependent manner. NAC inhibited the intracellular expression of AGE-HSA ROS increase, while inhibiting the secretion of VEGF in HPMC. CONCLUSION: AGE-HSA may induce intracellular ROS and promote the expression of VEGF in HPMC, which may lead to the increase of peritoneal neovascularization and ultimately lead to peritoneal loss of ultrafiltration.