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The study of inhibit the Slit/Robo pathway on vascular restenosis after angioplasty in rabbits / 实用医学杂志
The Journal of Practical Medicine ; (24): 1934-1937, 2016.
Article in Zh | WPRIM | ID: wpr-494484
Responsible library: WPRO
ABSTRACT
Objective To study the effect and mechanism of down-regulating Silt2/Robo 1 signaling pathway on rabbit iliac artery after angioplasty restenosis. Methods The 30 male New Zealand white rabbits were divided randomly into 3 groups , namely the blank group , the control group , and the experimental group , 10 rabbits in each group. Hign-fat feeding , the rabbits were produced endothelial denudation of iliac artery stenosis model. Another 4 weeks of feeding , percutaneous balloon angioplasty was performed. Then R5 antibody was injected into the abdominal cavity. After 4 weeks of feeding ,angiography again. The results of angiography was analysied by image workstation. The concentrations of Slit2 and Robo1 was detected by ELISA. The iliac artery tissue examined by HE staining. Results The rabbit iliac artery after angioplasty restenosis animal model was set up successfully. Compared with the control group and the experimental group , the serum concentration of Slit2 and Robo1 were significantly higher (P < 0.01) than the blank group. But in the experimental group, the Slit2 and Robo1 serum concentrations were significantly lower than those in the control group (P < 0.05) after R5 antibody intervention. The area ratio stenosis and diameter stenosis rate of iliac artery were reduced that confirmed by angiography. Conclusion The expression of Slit2/Robo1 was significantly higher in the rabbit model of vascular restenosis. R5 antibody can effectively inhibit the expression of Slit2/Robo1. Down regulation of Slit2/Robo1 signaling pathway in the treatment of restenosis after angioplasty in rabbits.
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Full text: 1 Index: WPRIM Language: Zh Journal: The Journal of Practical Medicine Year: 2016 Type: Article
Full text: 1 Index: WPRIM Language: Zh Journal: The Journal of Practical Medicine Year: 2016 Type: Article