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