Nrf2抵抗胰岛β细胞氧化损伤的作用机制

doi:10.7523/j.issn.2095-6134.2015.03.003

摘要/Abstract

摘要：

长期高血糖导致糖尿病患者的氧化应激,引起胰岛β细胞氧化损伤,但核转录因子Nrf2(NF-E2-related factor 2)抵抗胰岛β细胞氧化损伤的作用机制还不清楚.本研究用低浓度葡萄糖(LG, 5.6 mmol/L)、LG + H₂O₂和高浓度葡萄糖(HG, 27.6 mmol/L)分别处理小鼠胰岛NIT-1β细胞48 h,检测细胞内活性氧(ROS,reactive oxygen species)生成、胰岛素合成与分泌变化和Nrf2入核表达水平.研究发现,高糖诱导NIT-1β细胞的ROS生成,降低细胞合成与分泌胰岛素的水平,但Nrf2入核表达降低胰岛β细胞氧化应激.结果提示Nrf2入核表达可以抵抗高糖诱导的胰岛β细胞氧化损伤,改善细胞合成与分泌胰岛素的功能.

关键词: 高糖, 胰岛&beta, 细胞, 氧化应激, Nrf2

Abstract:

It is well known that hyperglycemia results in oxidative stress in diabetes mellitus, which causes pancreatic β cell dysfunction. However, this cytoprotective effect of Nrf2 on hyperglycemia-induced oxidative stress in pancreatic β cell is not fully understood. In the study, reactive oxygen species (ROS) and insulin synthesis and secretion as well as nucleus NF-E2-related factor 2 (Nrf2) expression in NIT-1β cells were determined after treatment of 48 h with low glucose (LG, 5.5 mmol/L), high glucose (HG, 27.6 mmol/L), or LG plus H₂O₂, respectively. We found that HG significantly induced ROS generation and decreased insulin synthesis and secretion in NIT-1β cells. However, HG-induced oxidative damage was improved by nucleus NF-E2-related factor 2 (Nrf2) expression. The results suggested that activation of Nrf2 through promotion of nuclear accumulation plays an important role in protection against hyperglycemia-induced oxidative injury.

Key words: hyerglycemia, pancreatic &beta, cell, oxidative stress, Nrf2

中图分类号:

587.1

宁梦丽, 丁文军, 张芳. Nrf2抵抗胰岛β细胞氧化损伤的作用机制[J]. 中国科学院大学学报, 2015, 32(3): 301-308.

NING Mengli, DING Wenjun, ZHANG Fang. Cytoprotective effect of Nrf2 expression on hyperglycemia-induced oxidative stress in pancreatic NIT-1β-cells[J]. , 2015, 32(3): 301-308.

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