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目的:观察葡萄糖降解产物甲基乙二醛(MGO)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MGO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ROS强度。结果:MGO能使细胞内ROS水平明显升高,呈浓度依赖效应;MGO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MGO导致的细胞内ROS升高,同时抑制HPMC中VEGF的分泌。结论:MGO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 glucose dehydrogenase (MGO) on the secretion of vascular endothelial growth factor (VEGF) and the role of intracellular reactive oxygen species (ROS) in human peritoneal mesothelial cells (HPMC). Methods: Different concentrations of MGO and antioxidant N-acyl-L-cysteine (NAC) were applied to the cells respectively. The expression of VEGF in HPMC was determined by RT-PCR and ELISA. Then the oxidation-sensitive fluorescent dye 2 , 7-dichlorodihydrofluorescein (DCFH) staining, flow cytometry intracellular ROS intensity. Results: MGO significantly increased intracellular ROS levels in a concentration-dependent manner. MGO promoted the expression of VEGF in HPMC both in time and dose-dependent manner. NAC inhibited the intracellular ROS increase induced by MGO, In the secretion of VEGF. CONCLUSION: MGO may induce ROS production in the cells and promote the expression of VEGF in HPMC, which may lead to the increase of peritoneal neovascularization and ultimately the peritoneal loss of ultrafiltration.