论文部分内容阅读
目的探讨诱导型一氧化氮合酶(iNOS)和内皮型一氧化氮合酶(eNOS)基因多态性与肝硬化门静脉高压的相关性。方法采用病例对照和聚合酶链反应-限制性片段长度多态性技术,检测106 例乙型肝炎后肝硬化患者(其中门静脉高压症65例)和108名健康对照者iNOS基因启动子-969G→C多态性及eNOS基因第七外显子894G→多态性,比较等位基因及基因型频率,并进行综合分析。结果在iNOS启动子969G→C多态性中,门静脉高压症组C等位基因和GC基因型频率比对照组显著升高(x2- 5.93,P<0.05)。GC基因型启动子的活性比GG基因型活性强。在eNOS的894G→T多态性中,T等位基因频率明显高于对照组(x2-3.91,P<0.05)。采用Logistic多元回归显示iNOS基因启动子-969G→C多态性及cNOS的894G→T多态性是门静脉高压症新的危险因素。结论iNOS启动子969G→C多态性和eNOS的894G→T多态性与门静脉高压症相关,是形成门静脉高压症新的危险因素。iNOS启动子-969G→C多态性可导致该基因启动子功能活性增强。
Objective To investigate the relationship between inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) gene polymorphisms and cirrhotic portal hypertension. Methods A case-control and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used in 106 patients with cirrhosis of the liver (including 65 cases of portal hypertension) and 108 healthy controls. The iNOS gene promoter-969G → C polymorphism and eNOS gene exon 7 894G → polymorphisms, alleles and genotypes were compared and analyzed. Results In the 969G → C polymorphism of iNOS promoter, the frequencies of C allele and GC genotype in patients with portal hypertension were significantly higher than those in controls (x2- 5.93, P <0.05). The GC genotype promoter is more active than the GG genotype. In eNOS 894G → T polymorphism, T allele frequency was significantly higher than the control group (x2-3.91, P <0.05). Logistic regression analysis showed that the iNOS promoter -969G → C polymorphism and cNOS 894G → T polymorphism were the new risk factors of portal hypertension. Conclusion The 969G → C polymorphism of iNOS promoter and 894G → T polymorphism of eNOS are associated with portal hypertension and are new risk factors for the formation of portal hypertension. The iNOS promoter -969G → C polymorphism leads to enhanced functional activity of this gene promoter.