基础医学与临床 ›› 2017, Vol. 37 ›› Issue (9): 1292-1296.

• 研究论文 • 上一篇    下一篇

慢性肾功能衰竭促进小鼠动静脉瘘内膜增生

江祥虎1,钟志鹏2   

  1. 1. 湖北省荆门市第二人民医院
    2. 荆门市第二人民医院
  • 收稿日期:2016-07-29 修回日期:2016-11-02 出版日期:2017-09-05 发布日期:2017-08-28
  • 通讯作者: 江祥虎 E-mail:275029009@qq.com

Chronic renal failure promotes intimal hyperplasia of arteriovenous fistula in mice

  • Received:2016-07-29 Revised:2016-11-02 Online:2017-09-05 Published:2017-08-28
  • Contact: xiang-Hu JIANG E-mail:275029009@qq.com

摘要: 目的 观察慢性肾功能衰竭对小鼠动静脉内瘘术后血管内膜增生的影响及单核细胞趋化蛋白-1(MCP-1)在内膜增生中的作用。方法 将24只C57小鼠分为对照组(n=12)与实验组(n=12),实验组行左肾全切及右肾上极动脉结扎,对照组行假手术,术后6周行左侧颈总动脉-颈外静脉端端吻合建立动静脉瘘(AVF)模型,AVF术后3周取瘘口静脉端血管组织。观察各组小鼠AVF内膜组织的病理改变及小鼠血液尿素氮(BUN)水平与内膜增生程度的关系;免疫组化法、RT-PCR法及Western印迹法检测各组静脉组织α平滑肌肌动蛋白(α-SMA)、ki-67、NF-κB及MCP-1的蛋白及mRNA的表达。结果 1)实验组较对照组小鼠血BUN水平明显上升(P<0.05),静脉端内膜增生更显著,管腔更狭窄(P<0.05)。2)实验组血管增生内膜α-SMA表达明显增加,血管平滑肌细胞(VSMC)增殖显著,NF-κB及MCP-1表达明显上升(均P<0.05)。3)MCP-1促进体外培养VSMC增殖。结论 慢性肾功能衰竭可明显增高NF-κB及MCP-1表达,从而促进动静脉瘘内膜增生及VSMC增殖。

关键词: 关键词:慢性肾功能衰竭, 动静脉瘘, 内膜增生, 单核细胞趋化蛋白-1

Abstract: Objective To observe the effect of chronic renal failure on the development of neointimal hyperplasia and the role of monocyte chemokine -1 (MCP-1) after arteriovenous fistula in mice. Methods we created AVF (common carotid artery to jugular vein in an end-to-end anastomosis) in mice with or without chronic renal failure (renal ablation or sham operation). The outflow of AVF was harvested at 3 weeks postoperative the vascular tissue. The pathological changes were observed. The level of blood urea nitrogen (BUN) levels and the degree of intimal hyperplasia were analysed . The protein and mRNA expression of alpha smooth muscle actin (SMA), Ki-67 ,NF-κB and MCP-1 were detected by immunohistochemistry , RT-PCR and Western blotting . Results 1) Compared with the control group, the blood BUN level of the experimental group was significantly higher and the intimal hyperplasia was more serious, meanwhile, the lumen was more narrow (P<0.05). 2) In the experimental group, the expression of α-SMA, ki-67, NF-κB and MCP-1 was significantly increased (P<0.05). 3) MCP-1 promoted the proliferation of vascular smooth muscle cells. Conclusion Chronic renal failure promote the development of neointimal hyperplasia, which may be related to the increase of MCP-1 expression.

Key words: Key words: chronic renal failure, arteriovenous fistula, neointimal hyperplasia, monocyte chemokine -1

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