对氧磷脂酶-1基因多态性与脑梗死的相关性研究

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目的探讨福建地区汉族人群动脉硬化性脑梗死患者血清对氧磷脂酶-1(PON-1)活性及其基因多态性与脑梗死的关系。方法把研究对象分为脑梗死组和对照组,用分光光度法检测这两组研究对象血清对氧磷脂酶-1(PON-1)活性,同时检测血浆氧化低密度脂蛋白(OX-LDL)、高密度脂蛋白胆固醇(HDL-C)的变化,并把这些指标与PON-1的活性作相关分析。采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术检测PON-1 192RR与55LL基因的多态性,用Logistic回归分析脑梗死组及对照组的基因型与其他危险因素的相关性。数据采用t检验及x~2检验。结果脑梗死组和对照组的PON-1活性均在已报道的中国人正常范围内,与对照组相比,脑梗死组血清PON-1活性明显降低(t=2.2142,P<0.05)。相关分析表明血PON-1活性与血OX-LDL呈负相关(r =-0.339,P<0.01),差异具有统计学意义,血PON-1活性与HDL-C无相关性。PCR结果表明PON-1 192基因的多态性在脑梗死组与对照组有明显不同,其中脑梗死组的RR基因型分布频率明显高于对照组(31.3% vs 24.6%,P=0.01,x~2=5.74),而PON-155基因的多态性在两组间差异无统计学意义(78.13% vs 76.78%,P=0.29,x~2=1.1)。分析还表明PON-1 192RR基因型的PON-1活性低于其它PON-1基因型,差异有统计学意义(P<0.001)。Logistic回归分析提示PON-1 192RR基因型是脑梗死的危险因素(OR=1.8,95% CI 0.16~5.08),高血压也是脑梗死的危险因素,而PON-155LL基因型可能不是脑梗死的危险因素。PON-1基因型与PON-1活性在高血压与非高血压组之间的差异无统计学意义。结论脑梗死组血清PON-1活性明显低于对照组,而且PON-1 192RR基因型分布频率高与对照组,与此同时,PON-1 192RR基因型的PON-1活性低于其它PON-1基因型,提示脑梗死组血清PON-1活性及PON-1 192RR基因多态性与脑梗死的发生有关,而高血压是脑梗死的独立危险因素。 Objective To investigate the relationship between plasma paraoxonase-1 (PON-1) activity and gene polymorphism and cerebral infarction in patients with arteriosclerotic cerebral infarction in Han nationality in Fujian province. Methods The subjects were divided into cerebral infarction group and control group. The levels of plasma paraoxonase-1 (PON-1) and serum levels of oxidized low density lipoprotein (OX-LDL) were detected by spectrophotometry. , High-density lipoprotein cholesterol (HDL-C) changes, and these indicators and PON-1 activity correlation analysis. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to detect the polymorphisms of PON-1 192RR and 55LL genes. Logistic regression was used to analyze the genotype and other risk factors of cerebral infarction group and control group Correlation. Data using t test and x ~ 2 test. Results The PON-1 activity of cerebral infarction group and control group were all within the reported range of normal in Chinese. Compared with control group, PON-1 activity of cerebral infarction group was significantly decreased (t = 2.2142, P <0.05). Correlation analysis showed that blood PON-1 activity was negatively correlated with blood OX-LDL (r = -0.339, P <0.01), the difference was statistically significant, blood PON-1 activity had no correlation with HDL-C. The results of PCR showed that the polymorphism of PON-1 192 gene was significantly different between cerebral infarction group and control group. The distribution frequency of RR genotype in cerebral infarction group was significantly higher than that in control group (31.3% vs 24.6%, P = 0.01, x ~ 2 = 5.74). The polymorphism of PON-155 gene was not significantly different between the two groups (78.13% vs 76.78%, P = 0.29, x ~ 2 = 1.1). Analysis also showed that PON-1 192RR genotype PON-1 activity was lower than other PON-1 genotypes, the difference was statistically significant (P <0.001). Logistic regression analysis showed that PON-1 192RR genotype was a risk factor for cerebral infarction (OR = 1.8,95% CI 0.16-5.08), and hypertension was also a risk factor for cerebral infarction. PON-155LL genotype may not be a risk factor for cerebral infarction factor. PON-1 genotype and PON-1 activity in hypertensive and non-hypertensive groups, the difference was not statistically significant. Conclusions The serum PON-1 activity in cerebral infarction group is significantly lower than that in control group, and the distribution frequency of PON-1 192RR genotype is higher than that in control group. Meanwhile PON-1 192RR genotype PON-1 activity is lower than other PON-1 Genotype, suggesting that PON-1 activity and PON-1 192RR gene polymorphism in patients with cerebral infarction were associated with the occurrence of cerebral infarction. Hypertension was an independent risk factor for cerebral infarction.
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