摘要
目的探讨血管紧张素Ⅱ(AngⅡ)水平与细胞外信号调节激酶(ERK)活化在人门静脉高压症(PHT)脾静脉血管病变中的作用及可能机制。方法选取乙型肝炎感染后肝硬化PHT患者26例为PHT组;选取因外伤性脾破裂行脾切除术患者10例为对照组。放射免疫分析法(RIA)检测脾静脉中AngⅡ水平;免疫组织化学法和蛋白免疫印迹法检测脾静脉中ERK的表达。结果PHT组脾静脉组织AngⅡ水平(248.91±48.31)ng/L,显著高于对照组(143.35±36.45)ng/L(P<0.01)。蛋白免疫印迹/免疫组织化学染色均显示PHT组脾静脉ERK表达较对照组明显增加。结论PHT时脾静脉组织AngⅡ水平升高,ERK表达增加。局部AngⅡ升高及ERK信号传导通路的激活可能与门静脉高压症的形成和维持有关。
Objective To investigate the role of local Ang Ⅱ level and extracellular signal-regulated kinase （ERK） activation in splenic vein vasculopathy in portal hypertension （PHT） and the possible mechanism of their action. Methods Twenty-six posthepatitic cirrhosis patients with portal hypertension served as the PHT group while 10 patients with traumatic spleen rupture during the same period as the control group. Local Ang Ⅱ level in splenic veins was determined by radioimmunoassay method. The expression of ERK in splenic veins was assayed by immunohistochemistry and western blot. Results The local Angll levels in the splenic veins of the PHT group were （248.91±48.31） ng·L^-1 , significantly higher than those in the control group （143.35±36.45） ng·L^-1 （P〈0.01）. The expression of ERK in the splenic vein of the PHT group was stronger than that of the control group （P〈0.01）. Conclusion The increase in Ang Ⅱ level and extracellular signal-regulated kinase expression in splenic veins may be critical for the formation and maintenance of portal hypertension.
出处
《福建医科大学学报》
2009年第6期460-462,共3页
Journal of Fujian Medical University
