Caveolin-1与内皮型一氧化氮合成酶在门静脉高压症性血管病变中的表达

CAVEOLIN-1 AND ENDOTHELIAL NITRIC OXIDE SYNTHASE EXPRESSIONS IN VASCULOPATHY OF PORTAL HYPERTENSION

目的检测肝硬化门静脉高压症病人的脾血管中小凹蛋白caveolin-1、内皮型一氧化氮合成酶(endothelial nitric oxide synthase,eNOS)的mRNA及蛋白表达水平的变化,探讨caveolin-1的表达对eNOS的影响。方法逆转录-聚合酶链反应(RT-PCR)方法检测27例肝硬化门静脉高压症病人脾静脉组织和20例脾外伤病人正常脾静脉血管中caveolin-1和eNOS的mRNA;Western Blot检测caveolin-1和eNOS的蛋白表达水平变化。结果肝硬化门静脉高压症组脾静脉Caveolin-1 mRNA与对照组脾静脉组织表达分别为(0.73±0.18)、(0.38±0.12),两组比较差异有显著性(p<0.05);肝硬化门静脉高压症组脾静脉eNOS mRNA为(0.23±0.11),显著低于对照组内脾静脉组织eNOS mRNA的表达(0.47±0.15)(p<0.05)。Western Blot检测caveolin-1在肝硬化门静脉高压症组脾静脉中较正常脾静脉中表达明显增强;eNOS在肝硬化门静脉高压症组脾静脉中呈低水平表达,较正常脾静脉中表达明显减少。结论肝硬化门静脉高压症组脾静脉中caveolin-1的过量表达及eNOS表达降低,导致NO合成减少,脾静脉血管阻力持续增加,及caveolin-1致静脉血管病理改变作用,共同作用致脾静脉出现对门静脉高压失代偿改变。

Objective To investigate the expression of mRNA and protein level of caveolin - 1 and endothelial nitric oxide synthase （eNOS） in vasculopathy of portal hypertension and to investigate the effect of caveolin - 1 on eNOS activity. Methods The expression of mRNA of caveolin - 1 and eNOS in splenic vein of PH patients and normal vascular were detected by RT - PCR analysis. Western Blot was used to detect the protein level of caveolin - 1 and eNOS. Results Levels of eNOS mRNA in splenic vein of PH group was （0. 23 ±0. 11 ）, significantly lower than that in control group（0. 47 ± 0. 15 ） （p 〈 0. 05 ）. Levels of caveolin - 1 mRNA in splenic vein of PH group was （0. 73 ±0. 18） ,significantly higher than that in control group（0. 51 ±0. 12） （p 〈0. 05）. Caveolin - 1 was more abundantly expressed in splenic vein of PH group than that in control group at protein level by western blot analysis, however eNOS was weakly expressed in splenic vein of PH group, significantly lower than that in control group. Conclusion Splenic vein of PH group, over - expression of caveolin - 1 may promote caveolin - 1 - eNOS binding and reduce the activity of eNOS, leading to impaired NO production and increased vasoconstriction, and splenic venous pressure. And caveolin - 1 as one of the factors in the pathogenesis of portal hypertensive vasculopathy,which can cause and advance decompensation of portal hypertensive vasculopathy.