VEGF及其受体在门静脉高压性胃病中的作用  

Role of vascular endothelial growth factor and its receptor mRNA in portal hypertensive gastropathy

作　　者：商中华[1] 张波[2] 陈海云[1] 董红霖[1] 王选[1] 祝庆华[1] 

机构地区：[1]山西医科大学第二临床医学院普外科,太原030001 [2]北京协和医院超声诊断科

出　　处：《山西医科大学学报》2008年第1期55-57,共3页Journal of Shanxi Medical University

基　　金：山西省青年科研基金资助项目(20031065)

摘　　要：目的探讨血管内皮生长因子(VEGF)及其受体1(f ms-like tyrosine kinase-1,FLT-1)和受体2(fetal liver kinese-1,FLK-1)mRNA在门静脉高压性胃病(PHG)动态变化中的作用。方法采用逆转录聚合酶链反应(RT-PCR)对44例肝硬化门静脉高压症患者PHG动态变化过程中病变部位VEGF,FLT-1及FLK-1mRNA的表达进行检测。结果44例病人首次胃镜检查轻度PHG23例,重度PHG11例。轻度PHG组VEGF,FLT-1,FLK-1mRNA(2.28±0.33,0.59±0.17,0.56±0.14)与无PHG组及正常对照组比较差异均有统计学意义(P<0.01);重度PHG组VEGF,FLT-1,FLK-1mRNA(3.48±1.02,0.68±0.20,0.71±0.18)与轻度PHG组、无PHG组及正常对照组比较差异均有统计学意义(P<0.01)。44例病人经6-12个月胃镜随访发现在无PHG组有4例发生PHG,轻度PHG组有7例发展为重度PHG,重度胃病组有3例转为轻度PHG。在PHG动态变化过程中VEGF,FLT-1,FLK-1mRNA的表达与PHG病变程度有明显相关性(P<0.01)。结论VEGF及其受体FLT-1,FLK-1过度表达是PHG胃黏膜损害的重要因素。Objective To explore the role of vascular endothelial growth factor （VEGF） and its receptor fms-like tyrosine kinase-1 （FLT-1）, fetal liver kinase-1 （FLK-1 ） mRNA in the development of portal hypertensive gastropathy（PHG）. Methods Forty-four portal hypertensive patients were investigated. The degree and the location of PHG were recorded. The expression of VEGF and its receptor FLT-1, FLK-1 mRNA were analyzed in gastric mucosa by reverse transcription-polymerase chain reaction （RT-PCR）. Results There are 23 patients with mild PHG and 11 patients with severe PHG at the first gastroscopic examination. After followed-up for 6 - 12 months, four patients appeared mild PHG in the patients without PHG, seven mild PHG patient turned to severe PHG, and three patients with severe PHG turned to mild PHG. VEGF and its receptor FLT-1, FLK-1 mRNA were all detected in the gastric mucosa, higher in moderate PHG patients than the patients without PHG and the normal controls[2.28 ±0.33, 0.59 ± 0.17,0.56 ± 0.14, respectively, P （0.01 ]. In the severe PHG patients, the expression of VEGF and its receptor FLT-1, FLK-1 mRNA were higher than the patients with moderate PHG and without PHG [3.48 ± 1.02,0.68 ± 0.20,0.71 ±0.18, respectively, P〈0.01]. During the dynamic changes of PHG, the expression of VEGF and its receptor FLT-1, FLK-1 mRNA also changed with its severity, they were positively related （P 〈0.01）. Conclusion The expression of VEGF and its receptor FLT-1, FLK-1 mRNA is up-regulated in the portal hypertensive gastric mucosa, which suggests that VEGF and its receptor FLT-1, FLK-1 mRNA may play an important role in the development of PHG.

关 键 词：高血压 门静脉 受体 血管内皮生长因子 逆转录聚合酶链反应 血管内皮生长因子 

分 类 号：R573[医药卫生—消化系统]