GUO Bei-bei, HUANG Jing, ZHU Que, et al. Effect of interleukin18 binding protein on neointimal proliferation after balloon injury and its possible mechanism. [J]. Journal of Chongqing Medical University 36(12):1427-1431(2011)
GUO Bei-bei, HUANG Jing, ZHU Que, et al. Effect of interleukin18 binding protein on neointimal proliferation after balloon injury and its possible mechanism. [J]. Journal of Chongqing Medical University 36(12):1427-1431(2011)DOI:
Effect of interleukin18 binding protein on neointimal proliferation after balloon injury and its possible mechanism
Objective:To investigate the effect and mechanism of interleukin 18 binding protein(IL-18BP) on neointimal proliferation of rabbit common iliac artery after balloon injury.Methods: New Zealand white male rabbits(n=48)were randomly divided into four groups:the control group
model group
low-dose treatment group and high-dose treatment group.All the rabbits were fed with hypercholesterol diet for 3 weeks
then IL-18BP was given to the rabbits in low-dose treatment group(5 μg) and high-dose treatment group(10 μg) by intravenous bolus injection during surgery
while the other two groups were treated with saline at the same volume.The rabbits were killed at 2 weeks and 4 weeks after balloon-injury.A total of 43 rabbits were used for this study.The common iliac artery was assayed by hematoxylin and eosin(HE) staining to investigate artery morphology and the thickness of arterial intima and media;the location and quantity of nuclear factor kappa B(NF-κB) were detected by immunohistochemistry and Western blot.Results: Compared with the control group
foam cells and intimal thickness in the model group were significantly increased;and those in low-dose treatment group and high-dose treatment group were decreased compared with the model group(P<0.05);compared with model group
the expression of NF-κB in low-dose and high-dose group was reduced significantly(P<0.01).Conclusion: IL-18BP can significantly decrease arterial neointimal hyperplasia after balloon-injury and the mechanism may be related to its inhibition of the expression of NF-κB.