《中国康复理论与实践》

《中国康复理论与实践》 ›› 2007, Vol. 13 ›› Issue (09): 845-847.

• 基础研究 • 上一篇    下一篇

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

马欣1a; 贾建平1a; 董秀敏1a; 温玫1b   

  1. 1.首都医科大学宣武医院a.神经内科;b.中心实验室,北京市 100053
  • 收稿日期:2007-08-24 出版日期:2007-09-01 发布日期:2007-09-01

Polymorphism of Nitric Oxide Synthase Gene and Nitric Oxide Production in Serum in Cerebral Infarction

MA Xin,JIA Jian-ping,DONG Xiu-min, et al   

  1. Department of Neurology, Xuanwu Hospital, Capital Medical University,Beijing 100053, China
  • Received:2007-08-24 Published:2007-09-01 Online:2007-09-01

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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。

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

Abstract: Objective To observe the polymorphism of nitric oxide synthase(NOS)gene and the changes of nitric oxide(NO)in cerebral infarct.Methods The prospective case-control study was employed.Cases contained 193 subjects with cerebral infarction of internal carotid artery system within 2 weeks.Controls contained 103 subjects which came from the normal health checkup.The polymorphism in intron 4 of endothelial nitric oxide synthase(eNOS)gene were detected.NO content was measured by Griess diazotization assay and NOS activity by enzynatic assay.Results There were 48 subjects with allele a in intron 4 of eNOS gene(eNOS4a)in cases and 12 in controls.The frequencies of eNOS4a in cases was higher than that in controls(χ2=8.86,P=0.003).Multivariate Logistic regression analysis confirmed that eNOS4a was an independent risk factors for cerebral infarction(P=0.032).NO production and NOS activity were 6.04(3.83～11.49)μmol/L,(2.97±1.47)U/ml,respectively in cases,and 6.89(4.64～12.43)μmol/L,(3.16±1.46)U/ml,respectively in controls.NO production in cases were significantly lower than that in controls(P=0.022).There was not differential in NOS activity between these two groups(P=0.517).NO production and NOS activity were 5.07(3.18～7.62)μmol/L,(2.77±1.13)U/ml,respectively in the subjects with eNOS4a,and 6.89(4.64～12.43)μmol/L,(3.12±1.54))U/ml,respectively in the subjects without eNOS4a.NO production in the subjects with eNOS4a were significantly lower than that in the subjects without eNOS4a(P=0.001).The NOS activities were not significantly different in subjects with or without eNOS4a(P=0.100).Conclusion eNOS4a possibly exerted some effects on cerebral infarction by diminishing NO.

Key words: nitric oxide, endothelial nitric oxide synthase, gene, polymorphism, cerebral infarction