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首页|期刊导航|中国临床保健杂志|胰高血糖素样肽-1受体在糖尿病大鼠周围神经中的表达及格列齐特的干预作用

胰高血糖素样肽-1受体在糖尿病大鼠周围神经中的表达及格列齐特的干预作用

沈玲玲 任明山 黄大可

中国临床保健杂志2012,Vol.15Issue(2):171-174,4.
中国临床保健杂志2012,Vol.15Issue(2):171-174,4.DOI:10.3969/J.issn.1672-6790.2012.02.022

胰高血糖素样肽-1受体在糖尿病大鼠周围神经中的表达及格列齐特的干预作用

Expression of GLP-1 receptor on diabetic peripheral neuropathy in diabetic rats and the intervention affect of gliclazide

沈玲玲 1任明山 1黄大可2

作者信息

  • 1. 安徽医科大学附属省立医院、安徽省立医院神经内科,合肥230001
  • 2. 安徽医科大学
  • 折叠

摘要

Abstract

Objective To investigate the expression and effect of glucagon-like peptide-1 receptor (GLP-1R) in sciatic nerve in diabetic rats and the intervention affect of gliclazide. Methods The rat model of type 2 diabetes was made by feeding a diet enriched with energy and ip low-dose streptozotocin. Histopathological changes of sciatic nerve in each group were observed by light microscope with HE dye. Expressions of GLP-1 R and caspase-3 in each group were detected by the immunohistochemistry. Results In DM rats,there was morphological changes of sci-atic nerve in the early 4 weeks by HE dye method, and the damage aggravated with the extension of DM course. The changes in gliclazide treated group were slighter than those of DM 8 weeks group in the corresponding period. In DM group,the expression of protein CLP-1R decreased significantly and the expression of protein Caspase-3 increased significantly in comparison with the NC group. In the treated groups,the expression of protein GLP-1R increased significantly and the expression of protein Caspase-3 decreased significantly in comparison with the DM group. Conclusion The changes of GLP-IR expression is related to the lesion degree of peripheral nerve in diabetes, gliclazide can increase GLR-K expression and inhabit the Caspase-3 expression.

关键词

糖尿病,2型/胰高血糖素样肽1/半胱氨酸天冬氨酸蛋白酶3/格列齐特/大鼠,Wistar

Key words

Diabetes mellitus, type 2/ Glucagon-like peptide 1/ Caspase 3/ Gliclazide/ Rats, Wistar

分类

医药卫生

引用本文复制引用

沈玲玲,任明山,黄大可..胰高血糖素样肽-1受体在糖尿病大鼠周围神经中的表达及格列齐特的干预作用[J].中国临床保健杂志,2012,15(2):171-174,4.

中国临床保健杂志

OACSTPCD

1672-6790

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