中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (2): 320-324.doi: 10.3969/j.issn.1673-8225.2012.02.030

• 组织构建基础实验 basic experiments in tissue construction • 上一篇    下一篇

莱菔硫烷诱导胰岛系INS-1细胞血红素氧合酶1的表达****★◆○

杨  怡1, 2○，于志文2, 3○，邵玮娟2○，金天如2○   

  1. 1宁夏医科大学教育部省部共建生育力保持重点实验室，宁夏回族自治区银川市 750004；2多伦多大学班庭糖尿病研究中心，加拿大安大略省多伦多市  M5G 1L7；   3中山大学广东省食物营养和健康重点实验室，广东省广州市 510080
  • 收稿日期:2011-10-08 修回日期:2011-11-12 出版日期:2012-01-08 发布日期:2012-01-08
  • 通讯作者: 通讯作者：金天如，博士，副教授。多伦多大学班庭糖尿病研究中心，加拿大安大略省多伦多市，M5G 1L7 tianru.jin@utoronto.ca
  • 作者简介:杨怡★，女，1973年生，甘肃省人，回族，2002年兰州大学医学院毕业，硕士，副教授，主要从事从事糖尿病抗氧化治疗机制研究。 yangyi73422@163.com
  • 基金资助:

    国家自然科学基金(81160103)，项目名称：硫辛酸活化转录因子Nrf2改善胰岛素抵抗的机制研究。宁夏回族自治区科技攻关国际科技合作计划(NXIC2011010)：项目名称：枸杞多糖改善胰岛素抵抗的功效研究。宁夏自然科学基金(编号，NZ1097)，项目名称：脂肪因子visfatin与代谢综合征的关系研究。宁夏医科大学特殊人才科研启动项目(编号，XT20)，项目名称：脂肪因子visfatin与代谢综合征的关系研究

Induction of heme oxygenas 1 by sulforaphane of INS-1 cells

Yang Yi1, 2, Yu Zhi-wen2, 3, Shao Wei-juan2, Jin Tian-ru2   

  1. 1Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Ningxia Medical University, Yinchuan  750004, Ningxia Hui Autonomous Region, China; 2Banting and Best Diabetes Centre, University of Toronto, Toronto  M5G 1L7, Ontario, Canada; 3Key Laboratory of Food Nutrition and Health, Sun Yat-sen University, Guangzhou  510080, Guangdong Province, China
  • Received:2011-10-08 Revised:2011-11-12 Online:2012-01-08 Published:2012-01-08
  • Contact: Jin Tian-ru, Doctor, Associate professor, Banting and Best Diabetes Centre, University of Toronto, Toronto M5G1L7, Ontario, Canada tianru.jin@utoronto.ca
  • About author:Yang Yi★, Master, Associate professor, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China; Banting and Best Diabetes Centre, University of Toronto, Toronto M5G1L7, Ontario, Canada yangyi73422@163.com
  • Supported by:

    the National Natural Science Foundation of China, No. 81160103*; the Ningxia Hui Autonomous Region Technology Research International Technology Cooperation Plan, No. NXIC2011010*; Natural Science Foundation of Ningxia, No. NZ1097*; the Startup Project in Research for Special Talents of Ningxia Medical University, No. XT20*

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摘要：

背景：莱菔硫烷可用于氧化应激相关疾病的治疗，血红素氧合酶是一种催化血红素降解的应激蛋白，已经成为预防氧化攻击的首选研究靶标之一。

目的：观察核因子E2相关因子2激动剂莱菔硫烷对大鼠胰岛细胞系INS-1细胞血红素氧合酶1蛋白表达作用及细胞保护机制。
方法：体外培养INS-1细胞，先用3 μmol/L莱菔硫烷进行干预培养3 h，再分别加入不同的胰岛素抵抗诱导剂葡萄糖氧化酶、地塞米松和葡萄糖胺刺激建立胰岛素抵抗细胞模型。
结果与结论：3 μmol/L莱菔硫烷处理INS-1细胞中血红素氧合酶1的表达增加(P < 0.05)，其效应在4 h后达到高峰(P < 0.05)。3 μmol/L莱菔硫烷的预处理可逆转由胰岛素抵抗诱导剂导致的血红素氧合酶1表达下调(P < 0.05)。而且在葡萄糖胺处理的INS-1细胞中，莱菔硫烷对血红素氧合酶1的表达改善与磷酸化PKB的表达上调具有正相关性(P < 0.05, r = 0.23)。结果证实，莱菔硫烷可能通过诱导核因子E2相关因子2介导的血红素氧合酶1表达，增强胰岛细胞抗氧化防御功能和抗损伤信号系统，从而达到拮抗胰岛素抵抗诱导剂对胰岛细胞的损伤作用。

关键词:

Abstract:

BACKGROUND: Sulforaphane (SFN) can be used for oxidative stress related disease’s treatment. Heme oxygenas1 (HO-1) is a kind of enzyme degrading stress hemoglobin protein and HO-1 has become the first choice of anti-oxidation process.
OBJECTIVE: To study the effect of SFN induced expression of HO-1 in a rat pancreatic beta cell line INS-1 and the potential cytoprotective mechanism of nuclear factor erythroid-related factor 2 (Nrf2).
METHODS: During the culture of INS-1 cells, 3 μmol/L SFN was incubated for 3 hours and then glucose oxidase, dexamethasone and glucosamine were added to establish insulin resistance models.
RESULTS AND CONCLUSION: The expression of HO-1 protein in INS-1 cells was increased after SFN (3μM) exposure, and reached the highest level after 4 hours exposure (P < 0.05). Decreased expression of HO-1 protein which was induced by inducers of insulin resistance could be reversed by SFN (3 μM) (P < 1 005). A positive correlation was found between the expression of HO-1 protein improved by SFN and the improved expression of protein kinase B phosphorylation in INS-1 cells treated with glucosamine (P < 0.05, r=0.23). SFN may enhance antioxidative defense in pancreatic beta cells through the induction of HO-1 via Nrf2 mediated transcription and enhance insulin signaling to protect beta cells from damaging.

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