罗梅, 燕诗琪, 曹桂秋, 王娟. PPARγ启动子甲基化与心肌梗死的相关性分析[J]. 循证医学, 2021, 21(2): 93-99. DOI: 10.12019/j.issn.1671-5144.2021.02.007
    引用本文: 罗梅, 燕诗琪, 曹桂秋, 王娟. PPARγ启动子甲基化与心肌梗死的相关性分析[J]. 循证医学, 2021, 21(2): 93-99. DOI: 10.12019/j.issn.1671-5144.2021.02.007
    LUO Mei, YAN Shi-qi, CAO Gui-qiu, WANG Juan. Analysis of the Correlation Between PPARγ Promoter Methylation and Myocardial Infarction[J]. Journal of Evidence-Based Medicine, 2021, 21(2): 93-99. DOI: 10.12019/j.issn.1671-5144.2021.02.007
    Citation: LUO Mei, YAN Shi-qi, CAO Gui-qiu, WANG Juan. Analysis of the Correlation Between PPARγ Promoter Methylation and Myocardial Infarction[J]. Journal of Evidence-Based Medicine, 2021, 21(2): 93-99. DOI: 10.12019/j.issn.1671-5144.2021.02.007

    PPARγ启动子甲基化与心肌梗死的相关性分析

    Analysis of the Correlation Between PPARγ Promoter Methylation and Myocardial Infarction

    • 摘要: 目的 分析过氧化物酶体增殖物激活受体γ(peroxisome proliferator-activated receptor gamma,PPARγ)启动子甲基化与心肌梗死的相关性。 方法 将研究对象分为心肌梗死组(110例)及对照组(102例),甲基化特异性实时荧光定量聚合酶链技术(methylation-specific real-time fluorescence quantitative polymerase chain technology,qMSP)分析两组PPARγ基因启动子甲基化水平,对比分析其与心肌梗死的相关性。 结果 心肌梗死组与对照组一般资料比较,差异均无统计学意义(P>0.05)。心肌梗死组中血糖,总胆固醇(total cholesterol,TC)、甘油三酯(triglyceride,TG)、低密度脂蛋白(low density lipoprotein,LDL-c)显著高于对照组(P<0.05)。心肌梗死组PPARγ启动子甲基化率显著高于对照组。无论甲基化发生在CpG-1或CpG-2,甲基化组的PPARγ mRNA表达水平均显著低于非甲基化组。心肌梗死组中PPARγ基因启动子区甲基化水平与TC、TG、LDL-c、脂蛋白a呈正相关,与高密度脂蛋白(high density lipoprotein,HDL-c)呈负相关,差异具有统计学意义(P<0.05);对照组中PPARγ基因启动子区甲基化水平与年龄呈正相关,且有统计学意义(P<0.05)。心肌梗死组的糖尿病患者中,PPARγ基因启动子区甲基化水平与狭窄程度呈正相关,且有统计学意义(P<0.05)。 结论 PPARγ启动子甲基化与心肌梗死存在相关性,其下降可能对心肌梗死起到保护作用,有望作为心肌梗死治疗的一个新靶点。

       

      Abstract: Objective To analyze the correlation between peroxisome proliferator-activated receptor gamma (PPARγ) promoter methylation and myocardial infarction. Methods The research subjects were divided into myocardial infarction group (110 cases) and control group (102 cases). Methylation-specific real-time fluorescence quantitative polymerase chain technology (qMSP) was used to analyze the methylation level of PPARγ gene promoter in the two groups and analysis its correlation with myocardial infarction. Results There was no significant difference in the general data between the myocardial infarction group and the control group (P>0.05). The blood glucose, total cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL-c) in the myocardial infarction group were significantly higher than those in the control group (P<0.05). The methylation rate of PPARγ promoter in the myocardial infarction group was significantly higher than that in the control group. Regardless of whether methylation occurs in CpG-1 or CpG-2, the expression level of PPARγ mRNA in the methylated group was significantly lower than that in the unmethylated group. In the myocardial infarction group, the methylation level of PPARγ gene promoter region was positively correlated with TC, TG, LDL-c, lipoprotein(a), and negatively correlated with high density lipoprotein (HDL-c). In the control group, the methylation level of PPARγ gene promoter region was positively correlated with age and was statistically significant (P<0.05). Among diabetic patients in the myocardial infarction group, the methylation level of the PPARγ gene promoter region was positively correlated with the degree of stenosis, and was statistically significant (P<0.05). Conclusions There was correlation between PPARγ promoter methylation and myocardial infarction, and its decrease may play a protective role in myocardial infarction, and it may be a new target for the treatment of myocardial infarction.

       

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