脑梗死患者一氧化氮合酶基因多态性及其对一氧化氮的影响

被引:3
作者
马欣 [1 ]
贾建平 [1 ]
董秀敏 [1 ]
温玫 [2 ]
机构
[1] 首都医科大学宣武医院神经内科
[2] 首都医科大学宣武医院中心实验室
关键词
一氧化氮(NO); 内皮型一氧化氮合酶(eNOS); 基因; 多态性; 脑梗死;
D O I
暂无
中图分类号
R743.3 [急性脑血管疾病(中风)];
学科分类号
摘要
目的观察脑梗死患者内皮型一氧化氮合酶(eNOS)基因多态性及一氧化氮(NO)变化情况。方法采用前瞻性病例对照研究,脑梗死组193例,均为发病2周内经头颅CT或MRI证实存在颈内动脉分布区梗死灶者,对照组103例为正常体检者。对两组eNOS基因4号内含子多态性进行测定,并采用Griess重氮化反应法和酶标法分别检测血清NO含量、NOS活性。结果脑梗死组eNOS基因4号内含子a等位基因(eNOS4a)携带者48例,对照组为12例,携带频率有显著性差异(χ2=8.86,P=0.003);经Logistic回归分析,eNOS4a携带是脑梗死的独立危险因素(P=0.032);脑梗死组NO产物浓度中位数为6.04(3.83~11.49)μmol/L,低于对照组6.89(4.64~12.43)μmol/L(P=0.022)。eNOS4a携带者NO产物浓度中位数为5.07(3.18~7.62)μmol/L,低于非携带者6.86(4.39~11.76)μmol/L(P=0.001)。脑梗死组NOS活性为(2.97±1.47)U/ml,对照组(3.16±1.46)U/ml,无显著性差异(P=0.517)。eNOS4a携带者NOS活性(2.77±1.13)U/ml,与非携带者(3.12±1.54)U/ml无显著性差异(P=0.100)。结论eNOS4a携带可能通过减少NO生成而在脑梗死发生过程中发挥作用。
引用
收藏
页码:845 / 847
页数:3
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