摘要
目的探讨肝硬化门静脉高压症(PHT)时局部血管紧张素原mRNA表达与核因子-κB(NF-κB)的活化在门静脉高压症性血管病变中的意义。方法采用逆转录聚合酶链反应(RT-0PCR)方法检测肝硬化门静脉高压症病人脾脏动、静脉组织和正常血管局部血管紧张素原mRNA的表达情况,用化学发光凝胶电泳迁移率实验(EMSA)方法检测局部NF-κB的活性。结果对照组内脾脏动、静脉组织局部血管紧张素原mRNA分别为0.23±0.12、0.18±0.10,显著低于肝硬化门静脉高压症组脾动脉、脾静脉组织局部血管紧张素原mRNA的表达0.48±0.21、0.43±0.16(P<0.05);对照组脾动、静脉局部NF-κB未被检测到明显的活性,而于肝硬化门静脉高压症组检测到显著具有活性的NF-κB表达(P<0.05)。结论肝硬化门静脉高压病人局部血管紧张素原mRNA表达增强,NF-κB的活化,可能是肝硬化门静脉高压症时内脏血管病变形成和发展的原因之一。
Objective To investigate the expression of local angiotensinogen mRNA and activation of local nuclear factor-κB in vasculopathy of portal hypertension and to discuss their role in the pathogenesis of portal hypertensive vasculopathy. Methods RT-PCR was used to detect the expression of local angiotensinogen mRNA in 28 specimens of splenic artery and vein obtained during operation of elective separation and amputation on 28 portal hypertension （PH） patients, 20 males and 8 females, aged 51.7 ± 10 （30-65）, and in 12 specimens of normal vessel from 12 patients undergoing splenectomy due to traumatic rupture of spleen. Chemiluminescent electrophoretic mobility shift assay （EMSA） was used to detect the activation of NF-κB in splenic artery and vein. Results The levels of local angiotensinogen mRNA in the splenic artery and vein of PH group were 0. 48 ± 0. 21 and 0. 43 ± 0. 16 respectively, both significantly higher than those in the control group （0.23 ± 0. 12 and 0. 18 ± 0. 10, both P 〈 0. 05 ）. There was no significant difference between the splenic artery and vein in the expression of local angiotensinogen mRNA in PH group. The activation levels of NF-κB in splenic artery and vein of the PH patients were 1.44 ± 0. 23 and 1.38 ±0.18 respectively, both significantly higher than those of the control group （0.19 ±0.20 and 0. 25 ± 0. 16 respectively, both P 〈 0. 05 ）. However, there was no significant difference in the activation levels of NF-KB between the splenic artery and vein in the PH patients （P 〉 0. 05 ）. Conclusion Local angiotensinogen and activation of NFκB maybe one of the factors in the pathogenesis of portal hypertensive vasculopathy, which can cause and advance portal hypertensive vasculopathy.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2005年第32期2283-2286,共4页
National Medical Journal of China
基金
国家自然科学基金资助项目(30170920)
