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目的探讨中国陕西地区汉族人群基质金属蛋白酶-2(matrix metalloproteinase-2,MMP-2)基因rs2285053及基质金属蛋白酶-9(MMP-9)基因rs3918242单核苷酸多态性与早发冠心病(premature coronary artery disease,PCAD)发病的关联性。方法应用聚合酶链反应-限制性片段长度多态性方法 ,检测92例PCAD患者(PCAD组)和95例年龄及性别相匹配的非冠心病者(对照组)的rs2285053(-735C/T)、rs3918242(-1562C/T)基因的单核苷酸基因多态性,判定其基因型并统计各基因型及等位基因的频率。ELISA法检测血浆MMP-9的水平。结果 MMP-2rs2285053位点多态性在PCAD组和对照组中的基因型分布和等位基因频率差异无统计学意义(χ2=1.33,P=0.249)。MMP-9rs3918242位点PCAD组C/T+T/T型高于对照组(χ2=6.22,P=0.013),T基因频率亦高于对照组,有显著性差异(χ2=7.75,P=0.005,OR=2.66)。早发急性冠脉综合征组(premature acute coronary syndrome,PACS)C/T+T/T型高于对照组,与早发稳定性心绞痛相比差异无统计学意义(χ2=9.11,P=0.003;χ2=2.29,P=0.13),早发稳定性心绞痛与对照组相比差异亦无统计学意义(χ2=1.3,P=0.254)。Logistic回归分析显示,MMP-9rs3918242位点携带T等位基因为PCAD发病的独立危险因素。结论 MMP-2rs2285053(-735)位点多态性可能与PCAD的发病无相关性,MMP-9rs3918242位点可能与PCAD及PACS发病相关,rs3918242(-1562)T等位基因可能是PCAD的遗传易感基因。
Objective To investigate the relationship between the rs2285053 of matrix metalloproteinase-2 (MMP-2) gene and rs3918242 of MMP-9 gene and the risk of premature coronary heart disease (CHD) in Han nationality in Shaanxi Province of China premature coronary artery disease, PCAD). Methods The polymorphisms of rs2285053 (-735C / T) in 92 PCAD patients and 95 age-matched and non-CHD patients (control group) were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) , Rs3918242 (-1562C / T) single nucleotide polymorphisms, to determine the genotypes and statistics of each genotype and allele frequencies. ELISA method for the determination of plasma MMP-9 levels. Results The genotype distribution and allele frequency of MMP-2 rs2285053 polymorphism in PCAD group and control group were not statistically different (χ2 = 1.33, P = 0.249). The frequency of T gene in PCAD group at MMP-9 rs3918242 site was higher than that in control group (χ2 = 6.22, P = 0.013), and the frequency of T gene was also significantly higher than that of control group (χ2 = 7.75, P = 0.005 , OR = 2.66). Premature acute coronary syndrome (PACS) C / T + T / T was higher than that of the control group, and there was no significant difference between the two groups (χ2 = 9.11, P = 0.003 ; χ2 = 2.29, P = 0.13). There was no significant difference in the incidence of early-onset stable angina compared with the control group (χ2 = 1.3, P = 0.254). Logistic regression analysis showed that the presence of T allele at MMP-9 rs3918242 was an independent risk factor for PCAD. Conclusion There is no correlation between MMP-2 rs2285053 (-735) polymorphism and the incidence of PCAD. The MMP-9 rs3918242 locus may be related to the pathogenesis of PCAD and PACS. The rs3918242 (-1562) T allele may be the genetic predisposition to PCAD Sense genes.