| 陈颉,冯晓红,黄琦.人参皂苷通过Nrf2/ARE信号通路干预波动性高糖致内皮细胞损伤的作用机制研究[J].浙江中西医结合杂志,2017,27(7): |
| 人参皂苷通过Nrf2/ARE信号通路干预波动性高糖致内皮细胞损伤的作用机制研究 |
| Mechanism of ginseng on apoptosis of human umbilical vein endothelial cells(HUVECs) exposed to intermittent high glucose by regulating Nrf2/ARE signaling |
| 投稿时间：2017-03-13 修订日期：2017-05-03 |
| DOI： |
| 中文关键词: 人脐静脉内皮细胞 Nrf2/ARE 波动性高糖 氧化应激 人参皂苷 |
| 英文关键词:HUVEC Nrf2/ARE Intermittent high glucose Oxidative stress Ginseng |
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| 中文摘要: |
| 目的 观察人参皂苷通过调控Nrf2/ARE信号通路,对波动性高糖所致内皮细胞损伤的影响,探讨人参皂苷起保护作用的部分机制。 方法 体外培养人脐静脉内皮细胞(HUVECs),分为对照组、波动性高糖模型组及人参皂苷低中高剂量治疗组。Western blot检测NF-E2相关因子2(Nrf2)的核转位及下游抗氧化蛋白血红素加氧酶-1(HO-1)、γ-谷氨酰半胱氨酸合成酶(γ-GCS)和醌氧化还原酶(NQO1)的表达；RT-PCR检测下游抗氧化蛋白HO-1、γ-GCS和NQO1的mRNA表达。瞬时转染Nrf2siRNA质粒, Western blot检测Nrf2总蛋白和核蛋白表达,及下游HO-1、γ-GCS和NQO1蛋白的表达。 结果 人参皂苷治疗后,HUVECs中的Nrf2核蛋白及下游抗氧化蛋白HO-1、γ-GCS和NQO1的表达均明显增强。瞬时转染Nrf2siRNA质粒后,人参皂苷的治疗作用消失。 结论 人参皂苷通过促进Nrf2核转位,调控Nrf2/ARE信号通路发挥其抗波动性高糖所致内皮细胞损伤的氧化应激损伤作用。 |
| 英文摘要: |
| Objective To explore the effect of ginseng on apoptosis of human umbilical vein endothelial cells(HUVECs) exposed to intermittent high glucose by regulating Nrf2/ARE signaling and study its mechanism. Methods HUVECs were cultured and divided into five groups: the control group, the intermittent high glucose group and the low, middle, high dosage of ginseng treatment group. The nucleoprotein of Nrf2 and its downstream antioxidant enzymes such as heme oxygenase-1(HO-1), γ-glutamyl cysteine synthetase(γ-GCS) and NAD(P)H quinone dehydrogenase 1 (NQO1) were detected by Western blot. The mRNA level of HO-1, γ-GCS and NQO1 were detected by RT-PCR. Western blot detected the nucleoprotein of Nrf2, and HO-1, γ-GCS and NQO1 after HUVECs transfected with Nrf2 siRNA. Results After the treatment of ginseng, the nucleoprotein of Nrf2 and level of mRNA, protein of HO-1, γ-GCS and NQO1 increased , while the treatment effect of ginsenoside disapperaed after HUVECs transfected with Nrf2 siRNA. Conclusion Ginseng took positive function of anti-oxidative stress on apoptosis of HUVECs exposed to intermittent high glucose by promoting nuclear translocation of Nrf2 and regulating Nrf2/ARE signaling. |
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