EFFECTS OF GLUCOSE AND ADVANCED GLYCATION END PRODUCTS ON OXIDATIVE STRESS IN MIN6 CELLS
EFFECTS OF GLUCOSE AND ADVANCED GLYCATION END PRODUCTS ON OXIDATIVE STRESS IN MIN6 CELLS
复制标题
葡萄糖和晚期糖基化终产物对 MIN6 细胞氧化应激的影响
DOI：
10.1170/140
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发表时间：
2010-01-01
影响因子：
1.6
通讯作者：
Su, Q.
中科院分区：
文献类型：
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作者：
Ge, Q-M;Dong, Y.;Su, Q.
探讨葡萄糖和糖基化终末产物（AGEs）诱导MIN6细胞氧化应激的机制。用MTT法检测细胞活力，用二氢乙锭（DHE）和二氢罗丹明123（DHR123）检测细胞内活性氧（ROS）的变化。使用流式细胞术通过测量平均荧光强度（MFI）来定量信号。用光泽精化学发光法测定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。MIN6细胞暴露于高糖或AGEs显著增加细胞内ROS的产生，并呈浓度和时间依赖性。与ROS产生的结果平行，MIN6细胞中的NADPH氧化酶由于葡萄糖或AGEs浓度的增加而被激活。高糖和AGEs通过激活NADPH氧化酶刺激ROS产生。因此，氧化应激可能损害胰腺β细胞功能，并导致糖尿病。
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.