摘要
为了探讨ADMA代谢酶基因多态性对个体罹患心脑血管疾病的机制,收集我院2012年~2016年经冠脉造影确诊的冠心病患者742例(试验组),同时收集我院体检中心的975例健康志愿者(对照组)。采集静脉血提取基因组DNA,采用PCR和限制性内切酶法检测DDAH1的基因位点多态性和酶联免疫法测定ADMA浓度。采用SPSS15.0软件进行数据统计分析,结果发现,试验组C144563T位点CC基因型频率及C等位基因频率均要明显高于对照组,其差异有统计学意义(p<0.05)。logistic回归分析结果显示,DDAH1基因CC基因型或144563C等位的个体患CHD的风险显著增加(OR=1.752,p=0.007)。试验组C^(143611)G位点GC基因型频率及C等位基因频率均要明显高于对照组,其差异有统计学意义(p<0.05)。logistic回归分析结果显示,DDAH1基因GC基因型或143611C等位的个体患CHD的风险显著增加(OR=1.890,p=0.004)。试验组人群血浆ADMA平均浓度为(3.07±0.51)μmol/mL,明显高于对照组人群血浆ADMA平均浓度(1.83±0.39)μmol/mL,差异有统计学意义(p=0.003<0.05)。C^(144563)T位点CC基因型与C^(143611)G位点GC基因型试验组个体血浆ADMA平均浓度((3.09±0.47)μmol/mL,(3.21±0.54)μmol/mL)均要显著高于对照组ADMA平均浓度((1.96±0.40)μmol/mL,(1.89±0.41)μmol/mL),其差异均有统计学意义(p=0.021,0.014<0.05)。我们推论且DDAH1基因的C^(144563)T位点与C^(143611)G位点与CHD密切相关,其影响机制可能是通过C^(144563)T位点与C^(143611)G位点基因型的改变而增高ADMA水平,从而导致CHD的发生与发展。
In order to investigate the mechanism of ADMA metabolic enzyme gene polymorphism on cardiovas- cular disease in individuals, we collected 742 cases of coronary heart disease patients diagnosed by coronary angiography from 2012 to 2016 in our hospital （the experimental group）, and 975 cases of healthy volunteers in our hospital （the control group）. The genomic DNA was extracted from venous blood, and the genetic locus of DDAH1 was determined by PCR and restriction enzyme method, and the ADMA concentration was detected by enzyme linked immunosorbent assay. SPSS15.0 software was used for statistical analysis, and it found that the CC genotype frequency and C allele frequencies in test group were significantly higher than those in the control group, and the difference was statistically significant （p〈0.05）. Logistic regression analysis showed that the risk of individuals with CC genotype or 144563C alleles in DDAH1 gene suffering from CHD was significantly increased the control group, and the difference was statistically significant （p〈0.05）. Logistic regression analysis showed that the risk of individuals with GC genotype or 143611C alleles in DDAH1 gene suffering from CHD was increased obviously （OR=1.890,p=0.004）. The average plasma ADMA concentration of the experimental group was （3.07±0.51） μmol/mL, which was significantly higher than that of the control group （1.83 ±0.39） μmol/mL, and the difference was statistically significant （p =0.003 〈0.05）. The average concentration of plasma ADMA of individuals with C144563T CC genotype and C1436HG GC genotype （（3.09±0.47） μmol/mL, （3.21 ±0.54） μmol/mL） were both higher than those of the control group （1.96±0.40） μmol/mL, （1.89±0.41） μmol/mL）, and the differences were statistically significant （p=0.021, 0.014〈0.05）. We concluded that C^144563T and C^143611G loci in DDAH1 gene was closely associated with CHD, whose influence mechanism might operate through increasing the level of ADMA by the cha
出处
《基因组学与应用生物学》
CAS
CSCD
北大核心
2017年第4期1325-1330,共6页
Genomics and Applied Biology
基金
重庆市中医院资助
