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SOCS3在糖尿病小鼠肾小管间质病变中的作用

高翔 邢玲玲 刘淑霞 杜云霞 李科军 刘思媛 刘青娟

临床与实验病理学杂志Issue(8):900-903,4.
临床与实验病理学杂志Issue(8):900-903,4.DOI:10.13315/j.cnki.cjcep.2015.08.014

SOCS3在糖尿病小鼠肾小管间质病变中的作用

Role of SOCS3 in tubulointerstitial injury of mice with diabetes

高翔 1邢玲玲 2刘淑霞 3杜云霞 3李科军 4刘思媛 3刘青娟3

作者信息

  • 1. 河北医科大学第二医院血管外科,石家庄050000
  • 2. 河北医科大学第二医院肾内科,石家庄050000
  • 3. 河北医科大学病理学教研室,石家庄 050017
  • 4. 河北省人民医院眼科,石家庄 050000
  • 折叠

摘要

Abstract

Purpose To investigate the role of SOCS3 on diabetic renal injury. Methods Male CD-1 mice were randomly divided into four groups:control group, diabetic group, empty plasmid vector transfection group and SOCS3 plasmid transfection group. The diabet-ic mice were induced by intraperitoneal injection of STZ at a dose of 150 mg/kg body weight. The mice of transfection group were re-ceived an injection of SOCS3 plasmid or empty vector at every 7 days thereafter. Specimens were collected at 12 week after STZ injec-tion. The morphological changes of tubular epithelial cells were observed by transmission electron microscope. RT-PCR and immuno-histochemistry were used to determine the mRNA and protein expression of CK18 and α-SMA. Western blotting analysis was used to determine the protein expression of SOCS3, p-STAT3, CK18 and α-SMA. Results SOCS3 overexpression in kidney down-regulated the levels of p-STAT3 andα-SMA but up-regulated the expression of CK18. Conclusion Overexpression of SOCS3 can ameliorate the tubular epithelial-mesenchymal transdifferentiation of diabetic mice via inhibiting the phosphorylation of STAT3.

关键词

糖尿病肾病/肾小管上皮细胞/细胞因子信号传导抑制蛋白3/信号转导和转录活化因子3

Key words

diabetic nephropathy/tubular epithelial cell/SOCS3/STAT3

分类

医药卫生

引用本文复制引用

高翔,邢玲玲,刘淑霞,杜云霞,李科军,刘思媛,刘青娟..SOCS3在糖尿病小鼠肾小管间质病变中的作用[J].临床与实验病理学杂志,2015,(8):900-903,4.

基金项目

教育部高等学校博士学科点专项科研基金(新教师类2013132320001) (新教师类2013132320001)

临床与实验病理学杂志

OA北大核心CSCDCSTPCD

1001-7399

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