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Protective effect of peroxiredoxin 2 on oxidative stress induced beta-cell toxicity in the pancreatic beta-cell line MIN6.

机译:过氧化物酶2对氧化应激诱导的胰腺β细胞系MIN6的β细胞毒性的保护作用。

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摘要

Type 1 and type 2 diabetes are characterized by an excessive loss of insulin producing β-cells. β-cells are particularly susceptible to increased oxidative stress induced apoptosis due to low expression of major antioxidants. Peroxiredoxin-2 (PRDX2) belongs to a group of antioxidants with antiapoptotic roles. Preliminary data indicate PRDX2 is expressed in the β-cells. Endogenous PRDX2 in the β-cell line MIN6 is found to decrease under oxidative stress conditions. I hypothesize that PRDX2 has a role in protecting β-cells against oxidative stress induced apoptosis. Overexpression or knockdown strategies were used to examine the role of PRDX2 in insulin-secreting MIN6 cells treated with various stimuli (cytokines, palmitate, streptozotocin) to induce apoptosis. Results showed that PRDX2 overexpression decreased oxidative stress induced apoptosis markers and cell death indicators, whereas knockdown of PRDX2 exaggerated oxidative stress induced toxicity. These findings suggest that PRDX2 plays a protective role in pancreatic β-cells under oxidative stress conditions.
机译:1型和2型糖尿病的特征是胰岛素分泌β细胞大量流失。由于主要抗氧化剂的低表达,β细胞特别容易受到氧化应激诱导的细胞凋亡的影响。 Peroxiredoxin-2(PRDX2)属于具有抗凋亡作用的抗氧化剂。初步数据表明PRDX2在β细胞中表达。发现β细胞系MIN6中的内源PRDX2在氧化应激条件下减少。我推测PRDX2在保护β细胞免受氧化应激诱导的细胞凋亡中起作用。使用过表达或基因抑制策略来检查PRDX2在经过各种刺激(细胞因子,棕榈酸酯,链脲佐菌素)处理以诱导细胞凋亡的胰岛素分泌性MIN6细胞中的作用。结果表明PRDX2过表达降低了氧化应激诱导的细胞凋亡标志物和细胞死亡指标,而PRDX2的敲低则夸大了氧化应激诱导的毒性。这些发现表明PRDX2在氧化应激条件下在胰腺β细胞中起保护作用。

著录项

  • 作者

    Zhao, Fang.;

  • 作者单位

    University of Toronto (Canada).;

  • 授予单位 University of Toronto (Canada).;
  • 学科 Biology Physiology.
  • 学位 M.Sc.
  • 年度 2011
  • 页码 81 p.
  • 总页数 81
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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