Kaempferol protects HIT-T15 Pancreatic Beta Cells from 2-deoxy-D-ribose-induced Oxidative Damage
Kaempferol protects HIT-T15 Pancreatic Beta Cells from 2-deoxy-D-ribose-induced Oxidative Damage
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DOI：
10.1002/ptr.2983
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发表时间：
2010-03-01
影响因子：
7.2
通讯作者：
Kim, Young Seol
中科院分区：
文献类型：
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作者：
Lee, Yun Jung;Suh, Kwang Sik;Kim, Young Seol
在 2 型糖尿病的进展过程中，葡萄糖毒性可能是导致β细胞进行性衰竭的重要原因。氧化应激是胰腺β细胞中葡萄糖毒性的一个重要方面，还原糖，例如2-脱氧-D-核糖（dRib），会产生活性氧。此外，类黄酮的许多生物特性可能与其抗氧化和自由基清除能力有关。因此，在本研究中，我们研究了山奈酚（一种黄酮醇）是否可以保护 β 细胞免受 dRib 诱导的氧化损伤。 HIT-T15细胞与不同浓度的dRib一起培养24小时。测量细胞存活率、产生的活性氧 (ROS) 量、细胞凋亡和脂质过氧化。研究发现 dRib 可以剂量依赖性地降低细胞存活率，从而显着增加细胞内 ROS 水平、细胞凋亡和脂质过氧化。然而，山奈酚 (10 μM) 抑制 dRib (20 mM) 诱导的细胞内 ROS、细胞凋亡和脂质过氧化。因此，我们证明山奈酚可减少 dRib 介导的 β 细胞损伤，从而干扰 ROS 代谢和对抗脂质过氧化的保护作用。我们的研究结果表明，山奈酚可保护 HIT-T15 细胞免受 dRib 诱导的相关氧化损伤。版权所有 (C) 2009 John Wiley & Sons, Ltd.
During the progression of Type 2 diabetes, glucose toxicity is likely to contribute importantly to progressive beta cell failure. Oxidative stress is an important aspect of glucose toxicity in pancreatic beta cells, and reducing sugars, such as 2-deoxy-D-ribose (dRib), produce reactive oxygen species. Furthermore, many of the biological properties of flavonoids are likely to be related to their antioxidant and free-radical scavenging abilities. Accordingly, in the present study, we investigated whether kaempferol (a flavonol) protects beta cells from dRib induced oxidative damage. HIT-T15 cells were cultured with various concentrations of dRib for 24h. Cell survivals, amounts of reactive oxygen species (ROS) generated, apoptosis, and lipid peroxidation were measured. dRib was found to dose-dependently reduce cell survival anti to markedly increase intracellular ROS levels, apoptosis, and lipid peroxidation. However, kaempferol (10 mu M) suppressed dRib (20 mM) induced intracellular ROS, apoptosis, and lipid peroxidation. So, we demonstrate that kaempferol reduces dRib-mediated beta cell damage interfering with ROS metabolism and protective effects against lipid peroxidation. Our findings indicate that kaempferol protects HIT-T15 cells from dRib-induced associated oxidative damage. Copyright (C) 2009 John Wiley & Sons, Ltd.