摘要
目的：探讨幽门螺杆菌（Helicobacter pylori,H.Pylori）感染与脂联素基因启动子–11391G/A、细胞外超氧化物歧化酶（extracellular superoxide dismutase,EC-SOD）基因多态性的交互作用以及与非酒精性脂肪性肝病（nonalcoholic fatty liver disease,NAFLD）的关系。方法：选择新乡医学院第一附属医院2010年6月至2014年7月收治的NAFLD患者600例,以600例健康体检者作为对照组,两组在年龄、性别、民族、籍贯和生活习惯方面无明显差异。以上述各组患者的外周血白细胞为样本,PCR检测脂联素基因启动子–11391G/A和EC-SOD基因多态性。14C-尿素呼气试验法（14C-urea breath test,14C-UBT）检测受检者H.Pylori与14C结合的每分钟衰变数（disntegration per minute,DPM）以判断H.Pylori感染情况;分析Pro12Ala,EC-SOD多态性与H.Pylori感染的交互作用。结果：–11391G/A（AA）基因型和EC-SOD（CG＋GG）基因型频率分布在病例组分别为50.67%和50.33%,在对照组分别为23.83%和24.17%,2组之间差异有统计学意义（–11391G/A：P=0.0051;EC-SOD：P=0.0057）。–11391G/A（AA）基因型患NAFLD的风险显著增加（OR=3.2822,95%CI：1.9170-5.2039）。EC-SOD（CG＋GG）基因型者患NAFLD的风险也显著增加（OR=3.1800,95%CI：1.7974-5.2391）。基因突变的协同分析发现：–11391G/A（AA）/EC-SOD（CG＋GG）基因型者在NAFLD组和对照组中的分布频率分别为25.50%和5.83%,2组之间差异有统计学意义（P=0.0039）。–11391G/A（AA）/EC-SOD（CG＋GG）基因型者患NAFLD的风险显著增加（OR=10.3190,95%CI：8.1869-20.5102）。病例组的H.Pylori感染率显著高于对照组的H.Pylori感染率（OR=3.1667,95%CI：1.9139-5.7443,P=0.0062）,H.Pylori感染与–11391G/A（AA）和EC-SOD（CG＋GG）基因型均有交互作用（–11391G/A：γ=1.8532,EC-SOD：γ=1.7899）。结论：携带–11391G/A（AA）和EC-SOD（CG＋GG）基因型的个体属NAFLD高危险人群,这些基因型和H.Pylori感染的交互作用促进了NAFLD的发生、发展,应当采取根除H.Pylori或调控基因表达的措施以达到有效预防NAFLD的目的。
Objective： To investigate the correlation between Helicobacter pylori（H. Pylori） infection and polymorphism of adiponectin gene promoter –11391G/A, extracellular superoxide dismutase（EC-SOD） gene in nonalcoholic fatty liver disease（NAFLD）.Methods： From June, 2010 to July, 2014, a hospital-based 1：1 matched case-control study was carried out, with 600 cases of NAFLD and 600 healthy people in the First Affiliated Hospital of Xinxiang Medical University. The genetic polymorphisms of adiponectin gene promoter –11391G/A and EC-SOD were analyzed by polymorphism-polymerase chain reaction（PCR） technique in peripheral blood leukocytes of the subjects. ^14C-urea breath test（^14C-UBT） was used to test ^14C disntegration per minute（DPM） for evaluating the infections status of H. Pylori. The synergistic effect between the two mutants and the gene-environment interaction of the genotypes with H. Pylori infection were analyzed.Results： The frequencies of –11391G/A（AA） and EC-SOD（CG＋GG） were 50.67% and 50.33% in NAFLD cases, 23.83% and 24.17% in healthy controls, respectively. Statistical tests showed significantly higher frequencies of –11391G/A（AA） and EC-SOD（CG＋GG） in the NAFLD group（–11391G/A： P=0.0051; EC-SOD： P=0.0057）. The risk of NAFLD with –11391G/A（AA） was significantly higher than those with –11391G/A（GG＋GA）（OR=3.2822, 95% CI 1.9170 to 5.2039）. The individuals who carried EC-SOD（CG＋GG） had a high risk of NAFLD（OR=3.1800, 95% CI 1.7974 to 5.2391）. Combined analysis of the polymorphisms showed that percentage of –11391G/A（AA）/EC-SOD（CG＋GG） in the NAFLD group was significantly higher than that in the control groups（25.50% vs 5.83%, P=0.0039）. The people who carried with –11391G/A（AA）/EC-SOD（CG＋GG） had a high risk of NAFLD（OR=10.3190, 95% CI 8.1869 to 20.5102）. The H. Pylori infection rate in the NAFLD group was signifi cantly higher than that in the control group（OR=3.1667, 95% CI 1.9139 to 5.7443, P=0.0062）, and statistical analysis suggested apositive correlation between H. Pylori infection and NAFLD with –11391G/A（AA） and EC-SOD（CG＋GG）（–11391G/A： γ=1.8532; EC-SOD： γ=1.7899）.Conclusion： These carriers of –11391G/A（AA） and EC-SOD（CG＋GG） genotypes may have a high risk of NAFLD, and the gene genotypes can interact with H. Pylori infection in the pathogenesis of NAFLD. Therefore, effective prevention measures for NAFLD should consider eradicating H. Pylori or regulating gene expression.
出处
《中南大学学报（医学版）》
CAS
CSCD
北大核心
2016年第4期359-366,共8页
Journal of Central South University ：Medical Science
基金
supported by the foundation of Henan Provincial Education Department,P.R.China(2011A320015)
