天津医药

天津医药 ›› 2015, Vol. 43 ›› Issue (4): 370-374.doi: 10.11958/j.issn.0253-9896.2015.04.010

• 实验研究 • 上一篇    下一篇

2 型糖尿病性动脉粥样硬化大鼠血浆VEGF、TGF-β1、 CTRP3 的表达及辛伐他汀的干预作用

王婉秋1，孙侃1△，靳瑾2，周婷3   

  1. 1石河子大学医学院第一附属医院内分泌代谢科（邮编832002）；2新疆医科大学第五附属医院内分泌代谢科；3石河子大学医学院第一附属医院中心实验室
  • 收稿日期:2014-09-10 修回日期:2014-11-25 出版日期:2015-04-15 发布日期:2015-04-13
  • 通讯作者: 孙侃 E-mail:wanqiu891009@126.com
  • 作者简介:王婉秋（1989），女，硕士在读，主要从事糖尿病及其慢性并发症研究

Serum levels of VEGF, TGF-β1 and CTRP3 in type II diabetic rat with atherosclerosis and the interventional mechanism of simvastatin

WANG Wanqiu1, SUN Kan1△, JIN Jin2, ZHOU Ting3   

  1. 1 Department of Endocrinology, The First Affiliated Hospital of Medical College, Shihezi University, Shihezi, Xinjiang 832002, China; 2 Department of Endocrinology, The Fifth Affiliated Hospital of Xinjiang Medical University, Urumqi; 3 Central Laboratory, The First Affiliated Hospital of Medical College, Shihezi University, Shihezi
  • Received:2014-09-10 Revised:2014-11-25 Published:2015-04-15 Online:2015-04-13
  • Contact: SUN Kan E-mail:wanqiu891009@126.com

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摘要： 摘要：目的观察2 型糖尿病性动脉粥样硬化大鼠血浆血管内皮生长因子（VEGF）、转化生长因子β1（TGF- β1）、C1q/TNF 相关蛋白3（CTRP3）的表达及辛伐他汀的干预作用。方法将SD 大鼠随机分为正常饮食（NC）组（n＝8）、高脂饮食（HFD）组（n＝8）、高脂干预（HFD+S）组（n＝8）、模型（M）组（n＝18）、模型干预（M+S）组（n＝16）。采用链脲佐菌素＋维生素D3＋高脂饮食建立糖尿病动脉粥样硬化大鼠模型，HFD+S、M+S 组用辛伐他汀溶液20 mg/(kg·d) 灌胃进行干预，蒸馏水20 mL/(kg·d)灌胃作为对照。测定各组大鼠空腹血糖（FPG）、血脂、空腹胰岛素（FINS）、VEGF、 TGF-β1、CTRP3 的水平。结果M 组动脉病理可见明显粥样斑块，M+S 组病变较M 组明显减轻。HFD 组VEGF、 TGF-β1 及CTRP3 高于NC 组；M 组VEGF、TGF-β1 高于NC 组，VEGF 高于HFD 组，CTRP3 低于HFD 组。辛伐他汀干预后，HFD+S 组TGF-β1、CTRP3 高于HFD 组，M+S 组VEGF 低于M 组，且TGF-β1、CTRP3 均高于M 组（P＜ 0.05）。结论VEGF、TGF-β1、CTRP3 可能参与糖尿病性动脉粥样硬化的发生，辛伐他汀除降脂外，还能下调 VEGF、上调TGF-β1、CTRP3 表达，并对糖尿病性动脉粥样硬化发挥保护作用。

关键词: 糖尿病, 2 型；动脉粥样硬化；血管内皮生长因子类；转化生长因子β1；C1q/TNF 相关蛋白3；辛伐他汀

Abstract: Abstract：Objective To investigate the serum expressions of vascular endothelial growth factor (VEGF), transforming growth factor-β1 (TGF-β1) and C1q/tumor necrosis factor-related protein 3 (CTRP3) in type II diabetic rats with atheroscle⁃ rosis and to undermine the interventional mechanism of simvastatin. Methods SD rats were randomly divided into normal diet (NC) group (n＝8), high-fat diet (HFD) group (n＝8), high-fat diet intervention (HFD+S) group (n＝8), model (M) group (n＝18) and model intervention (M+S) group (n＝16). The diabetic atherosclerosis model was established by streptozotocin (STZ)＋Vitamin D3（VitD3）＋High-fat diet. The group HFD+S and group M+S rats were administrated with simvastatin at 20 mg/（kg·d）intragastrically as intervention while distilled water [20 mL/（kg·d）] were given to other groups. Serum levels of fasting plasma glucose（FPG）, blood lipid, fasting insulin（FINS）, VEGF, TGF-β1 and CTRP3 were compared between each groups. Results Characteristics of atheromatous plaque were seen in group M and group M + S whose pathological change were markedly attenuated compared to group M. Serum levels of VEGF, TGF-β1 and CTRP3 were significantly high⁃ er in rats from Group HFD than those in rats from group NC. Serum levels of VEGF and TGF-β1 were significantly higher in rats from Group M than those in rats from group NC. Serum level of VEGF was significantly higher in rats from Group M than it in rats from group HFD. Serum level of CTRP3 was significantly lower in rats from Group M than it in rats from group HFD. Moreover, serum levels of TGF-β1 and CTRP3 were significantly higher in rats from Group HFD+S than those in rats from group HFD after the intervention with simvastatin. Serum level of VEGF was significantly lower in rats from Group M+S than it in rats from group M, and serum levels of TGF-β1 and CTRP3 were significantly higher in rats from group M+S than those in rats from group M after the intervention with simvastatin. Conclusion VEGF, TGF-β1 and CTRP3 may partici⁃ pate in development of diabetic atherosclerosis. In addition to its hypolipidemic role, Simvastatin can also down regulate se⁃ rum level of VEGF and up regulate serum levels of TGF-β1 and CTRP3 to exert a significant protective effect on diabetic atherosclerosis.

Key words: diabetes mellitus, type 2；atherosclerosis, vascular endothelial growth factors；transforming growth factor beta1；C1q/tumor necrosis factor-related protein 3；Simvastatin