血管内放射治疗对血管成形术后再狭窄及核因子-кB活性的影响

Effects of Endovascular Brachytherapy on Restenosis After Angioplasty and Nuclear Factor-кB

目的观察32P液体球囊血管近距离照射预防血管成形术后再狭窄的量效关系及其对核转录因子核因子кB(NFкB)活性的影响,以探讨其防治再狭窄的可能作用机制。方法24只大耳白兔,建立兔双侧髂动脉粥样硬化狭窄模型,随机选择一侧髂动脉血管成形术并分别给予91Gy组、218Gy组和334Gy组32P液体球囊血管照射治疗(每组n=8),另一侧髂动脉灌注造影剂,作为自身对照(对照组,n=24)。术后5周行血管造影并取材进行光镜观察、NFкB、胰岛素样生长因子1(IGF1)免疫组织化学染色,用计算机图像分析测量新生内膜面积、中膜面积、管腔面积及免疫组化染色阳性面积百分比。结果①光镜观察91Gy组与对照组比病变无明显差异;218Gy组内弹力膜完整无明显断裂;管腔轻度狭窄,新生内膜面积明显减小,内膜层泡沫样细胞及脂质沉积均不明显;中膜平滑肌呈轻度增厚,排列轻度紊乱;334Gy组内弹力膜破坏,管腔明显狭窄,内膜可见大量泡沫细胞及脂质沉积,大量炎性细胞浸润及细胞外基质不定形物质沉积,中膜平滑肌明显萎缩变薄,其中4例血管腔内可见血栓形成。②免疫组化染色91Gy组NFкB、IGF1蛋白表达与对照组无明显差异(P>005);218Gy组NFкB、IGF1蛋白表达量中等,呈灶状散在分布于内皮细胞、平滑肌细胞及泡沫细胞,与对照组相比有明显差异(P<001);③334Gy?

Objective:To observe the dose effect relation of endovascular brachytherapy to 32 P preventing restenosis after angioplasty,and to clarify the possible mechanisms of irradiation therapy for reducing restenosis Methods: The double iliac artery atherosclerotic stenosis model was set up in 24 rabbits Angioplasty was performed and 32 P brachytherapy at one side was randomly given,in doses of 9 1Gy,21 8Gy and 33 4Gy,respectively The other side served as self controled After 5 weeks,iliac artery angiography was performed,pathological sections of iliac arteries were observed with light microscope,nuclear factor кB(NF кB) and insulin like growth factor 1 were stained using immunohistochemical technique We also measured the neointima areas,lumen areas,media areas and the percentage of positive areas by computer analysis of photomicrograms Results: There were no obvious changes in the 9 1Gy group In the 21 8Gy group,the proliferation and migration of smooth muscle cells were significantly suppressed and the lumen areas did not decrease However, the thicked neointima made the cavity obvious stenosis, and the media smooth muscle shrinked and thinned in the 33 4Gy group Arterial thrombosis occurred in 4 vessels tients Conclusions:Endovascular brachytherapy with 32 P filled balloon catheter system could prevent restenosis after angioplasty The mechanism may be responsibie for the inhibition of the activities of NF кB and its target gene,thus reducing the proliferation and migration of smooth muscle cells