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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 cardiovascular disease in individuals, 742 coronary heart disease patients (experimental group) diagnosed by coronary angiography in our hospital from 2012 to 2016 were collected. At the same time, 975 healthy volunteers (control group). Venous blood was collected for genomic DNA extraction. DDAH1 gene polymorphism was detected by PCR and restriction enzyme digestion, and ADMA concentration was determined by ELISA. SPSS15.0 software was used to analyze the data. The results showed that CC genotype frequency and C allele frequency of C144563T site in experimental group were significantly higher than those in control group (p <0.05). Logistic regression analysis showed that the risk of CHD was significantly increased in individuals with CC genotype DDAH1 or allele 144563C (OR = 1.752, p = 0.007). The GC genotype frequency and C allele frequency of C site at 143611 in experimental group were significantly higher than those in control group (p <0.05). Logistic regression analysis showed that the risk of CHD was significantly increased in individuals with genotype D or GC genotype 143611C (OR = 1.890, p = 0.004). The average concentration of plasma ADMA in the test group was (3.07 ± 0.51) μmol / mL, which was significantly higher than that of the control group (1.83 ± 0.39) μmol / mL. The difference was statistically significant (p = 0.003 <0.05). Mean plasma concentrations of ADMA (3.09 ± 0.47μmol / mL, (3.21 ± 0.54) μmol / mL) in C genotype at 144563 T site and genotype GC genotype at 143611 G site were (1.96 ± 0.40) μmol / mL, (1.89 ± 0.41) μmol / mL), the difference was statistically significant (p = 0.021, 0.014 <0.05). We conclude that the C ~ (144563) T site and the C ~ (143611) G site of DDAH1 gene are closely related to CHD. The possible mechanism is that C ~ (144563) T site and C ~ (143611) G site Point genotype changes and increased ADMA levels, leading to the occurrence and development of CHD.