摘要
目的:探讨超声破坏微泡联合粒细胞集落刺激因子(G-CSF)刺激大鼠梗死心肌血管内皮生长因子(VEGF)分泌、促进血管新生的有效性.方法:心肌梗死模型Wistar大鼠40只,随机分为:超声+微泡造影剂+G-CSF(A组);超声+微泡造影剂组(B组);单纯G-CSF组(C组);单纯手术(SA)组(D组).于治疗后2 wk处死大鼠取材,采用免疫组化法检测心肌组织CD34的表达,并在显微镜下计数心肌内新生血管密度(MVD).采用酶联免疫吸附法(EUSA)检测心肌组织内VEGF蛋白表达情况.结果:免疫组化显示A组心肌组织中有大量CDM表达,新生血管最多,MVD计数为(231±24)个/高倍镜视野,明显高于B组(148±19),C组(100±12),D组(86±8)个/高倍镜视野,差异具有统计学意义(P<0.05).ELISA检测结果显示A组心肌组织中VEGF蛋白表达量为(3.14±0.21)ng/S,明显高于B组(2.56±0.17),C组(1.91±0.14),D组(0.97±0.11)ng/g,差异具有统计学意义(P<0.05).结论:超声破坏微泡可刺激缺血心肌内源性VEGF分泌,促进心肌血管新生,联合G-CSF能明显增强其血管新生作用.
Abstract
AIM: To explore whether ultrasound-targeted micro-bubble destruction ( US/MB) combined with granulocyte colony-stimulating factor ( G-CSF) can facilitate secretion of vascular endothelial growth factor ( VEGF) and angiogenesis of the infarcted myocardium in rats. METHODS: Forty myocardial infarction Wistar rats models were randomly divided into 4 groups: US/MB + G-CSF treatment group (A); US/MB alone treatment group ( B); G-CSF alone treatment group (C); and surgery alone (SA) group (D). Two weeks later, the rats were killed and the myocardia were harvested. The CD34 expression was detected by immunohistochemistry, and microvessel density ( MVD) was counted in high-power field ( HPF) under microscope. The VEGF expression in myocardium was detected by ELISA. RESULTS: There was significant CD34 expression in the myocardium of group A, and the MVD was higher in group A [ (231 ±24)/HPF] than in group B[( 148 ±19)/HPF], C[ (100 ±12)/HPF] and [(86 ±8)/HPF](P<0.05). The content of VEGF in the myocardium of group A[ (3. 14 ±0. 21) ng/g] was higher than those in group B[ (2.56 ±0.17)ng/g], C[ (1.91 ±0. 14)ng/g ], and D[(0.97±0.11)ng/g](P<0.05). CONCLUSION: US/MB can facilitate the endogenous secretion of VEGF and accelerate the vascularization to the infarcted myocardium in rats. Pretreatment with G-CSF can augment the angiogenic effect of US/MB.
基金项目
国家自然科学基金重点项目(30430230)
国家高技术研究发展计划(863计划)(2006AA0224F0)
NETL
NSTL
维普
万方数据