中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (2): 313-316.doi: 10.3969/j.issn.1673-8225.2011.02.030

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

L6大鼠成肌细胞胰岛素信号传导通路中磷脂酰肌醇3激酶、蛋白激酶B和葡萄糖转运蛋白4的表达

任小燕1，闫朝丽1，胡康洪2，苏秀兰3，李彩萍1，张嘉玲3   

  1. 内蒙古医学院附属医院，1内分泌科，3临床医学研究中心，内蒙古自治区呼和浩特市 010059；2中国科学院武汉病毒研究所病毒RNA结构与功能关系学科组，湖北省武汉市  430040
  • 收稿日期:2010-11-11 修回日期:2010-12-04 出版日期:2011-01-08 发布日期:2011-01-08
  • 通讯作者: 闫朝丽，女，1968年生，博士，教授，内蒙古医学院附属医院内分泌科，内蒙古自治区呼和浩特市 010059 aliceyzl@126. com
  • 作者简介:任小燕★，女，1984年生，汉族，内蒙古医学院在读硕士，主要从事内分泌性高血压的研究。 violetrenxiaoyan@126.com
  • 基金资助:

    课题受春晖计划(Z2007-1-01008)和内蒙古医学院第一附属医院重大课题(NYFYZD 201005)资助。

Expressions of phosphoinositide-3-kinase, protein kinase B and glucose transporter 4 involved in insulin signal conduction pathway in L6 rat skeletal myoblasts 

Ren Xiao-yan1, Yan Zhao-li1, Hu Kang-hong2, Su Xiu-lan3, Li Cai-ping1, Zhang Jia-ling3   

  1. 1Department of Endocrinology, 3Research Center of Clinical Medicine, Affiliated Hospital of Inner Mongolia Medical College, Hohhot  010059, Inner Mongolia Autonomous Region, China; 2Research Group of Viral RNA Structure and Function Relationships, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan  430040, Hubei Province, China
  • Received:2010-11-11 Revised:2010-12-04 Online:2011-01-08 Published:2011-01-08
  • Contact: Yan Zhao-li, Doctor, Professor, Department of Endocrinology, Affiliated Hospital of Inner Mongolia Medical College, Hohhot 010059, Inner Mongolia Autonomous Region, China aliceyzl@126.com
  • About author:Ren Xiao-yan★, Studying for master’s degree, Department of Endocrinology, Affiliated Hospital of Inner Mongolia Medical College, Hohhot 010059, Inner Mongolia Autonomous Region, China violetrenxiaoyan@ 126.com
  • Supported by:

    the Chunhui Plan, No. Z2007-1-01008; Major Issue of Affiliated Hospital of Inner Mongolia Medical College, No. NYFYZD 201005

PDF

314

被引次数

2

摘要：

背景：血管紧张素Ⅱ可损伤胰岛素信号中的下游信号分子引起胰岛素抵抗，但其机制不清。
目的：观察血管紧张素Ⅱ对L6大鼠成肌细胞胰岛素信号传导通路中磷脂酰肌醇3激酶、蛋白激酶B和葡萄糖转运蛋白4的影响。
方法：L6细胞培养及诱导分化肌管，根据干预措施不同实验分为对照组、胰岛素组、胰岛素+血管紧张素Ⅱ组及胰岛素+血管紧张素Ⅱ+H89组。采用RT-PCR检测4组磷脂酰肌醇3激酶、蛋白激酶B mRNA表达，免疫荧光检测胰岛素受体底物1、酪氨酸磷酸化胰岛素受体底物1、葡萄糖转运蛋白4表达。
结果与结论：胰岛素组、胰岛素+血管紧张素Ⅱ组及胰岛素+血管紧张素Ⅱ+H89组的磷脂酰肌醇3激酶mRNA表达均较对照组显著升高(P < 0.05)。各组间蛋白激酶B mRNA表达差异无显著性意义(P> 0.05)。相比对照组，其余3组间胰岛素受体底物1、酪氨酸磷酸化胰岛素受体底物1和葡萄糖转运蛋白4(膜蛋白)表达均升高(P < 0.05)；胰岛素+血管紧张素Ⅱ+H89组酪氨酸磷酸化胰岛素受体底物1和葡萄糖转运蛋白4表达低于胰岛素组但高于胰岛素+血管紧张素Ⅱ组(P < 0.05)。结果显示，血管紧张素Ⅱ在骨骼肌细胞中通过JAK2-PKA通路引起胰岛素下游信号传导受阻，葡萄糖转运蛋白4表达减少，葡萄糖转运障碍，进而导致胰岛素抵抗。

关键词: 血管紧张素Ⅱ, 胰岛素抵抗, 磷脂酰肌醇3激酶, 蛋白激酶B, 葡萄糖转运蛋白4

Abstract:

BACKGROUND: Angiotensin Ⅱ (AngⅡ) can damage the insulin signal in the downstream signaling molecules and induce insulin resistance, but the specific mechanism remain poorly understood.
OBJECTIVE: To study the effects of AngⅡ on proteins involved in insulin signal conduction pathway including phosphoinositide-3-kinase (PI3K), protein kinase B (PKB) and glucose transporter 4 (GLUT4) in L6 rat skeletal myoblasts.
METHODS: L6 rat myoblasts cultured and differentiated myotubes and were divided into 4 groups: control group, insulin group, insulin+AngⅡ group and insulin+AngⅡ+H89 group according to AngⅡ or H-89 different interventions. PI3K and PKB mRNA were detected by RT-PCR; expressions of insulin resistance substance 1 (IRS1), Ptyr-IRS1 and GLUT4 (membrane protein) were detected by immunofluorescence.
RESULTS AND CONCLUSION: The expression of PI3K mRNA were increased in the insulin, insulin+AngⅡand insulin+AngⅡ+H89 groups than that of the control group (P < 0.05). PKB total mRNA among the 4 groups was not significantly different (P > 0.05). Compared with the control group, expressions of IRS1, Ptyr-IRS1 and GLUT4 (membrane protein) were increased in the other three groups (P< 0.05). Ptyr-IRS1 and GLUT4 (membrane protein) expressions in the insulin+AngⅡ+H89 group was lower than those of the insulin group but higher than those of insulin+AngⅡ group (P < 0.05). The results demonstrated that: AngⅡ blocks insulin signaling downstream via JAK2-PKA signaling pathway, reduces GLUT4 expression and causes glucose transport hindrance, therefore, induces insulin resistance.

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