Ge Q-M, Dong Y, Su Q
Department of Endocrinology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Cell Mol Biol (Noisy-le-grand). 2010 Feb 9;56 Suppl:OL1231-8.
To explore the mechanism of oxidative stress induced by glucose and advanced glycation end products (AGEs) in MIN6 cells. The MIN6 cells were exposed to various concentrations of glucose or AGEs for some time, MTT assay was used to evaluate the cell viability, reactive oxygen species (ROS) was monitored using intracellular ROS capture Dihydroethidium (DHE) and dihydrorhodamine123 (DHR123). The signal was quantified using flow cytometry by measuring the mean fluorescent intensity (MFI). The NADPH oxidase activity was measured by chemiluminescence with lucigenin. Treatment of high glucose or AGEs decreased cell viability in a dose- and time- dependent fashion. Exposure of MIN6 cells to high glucose or AGEs significantly increased intracellular ROS production in a concentration- and time- dependent manner. In parallel with the results of ROS production, the NADPH oxidase in MIN6 cells was activated due to increased glucose or AGEs concentration. High glucose and AGEs stimulated ROS production via the activation of NADPH oxidase. The oxidative stress may consequently impair pancreatic beta-cell function and contribute to diabetes mellitus as a result.
探讨葡萄糖和晚期糖基化终产物（AGEs）诱导MIN6细胞氧化应激的机制。将MIN6细胞暴露于不同浓度的葡萄糖或AGEs一段时间，采用MTT法评估细胞活力，使用细胞内活性氧捕获剂二氢乙锭（DHE）和二氢罗丹明123（DHR123）监测活性氧（ROS）。通过测量平均荧光强度（MFI），使用流式细胞术对信号进行定量。用光泽精通过化学发光法测量NADPH氧化酶活性。高糖或AGEs处理以剂量和时间依赖性方式降低细胞活力。将MIN6细胞暴露于高糖或AGEs会以浓度和时间依赖性方式显著增加细胞内ROS的产生。与ROS产生的结果一致，由于葡萄糖或AGEs浓度增加，MIN6细胞中的NADPH氧化酶被激活。高糖和AGEs通过激活NADPH氧化酶刺激ROS产生。氧化应激可能因此损害胰腺β细胞功能，并导致糖尿病。
