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目的:分析OSAHS与肿瘤坏死因子(TNF)-α及锌指蛋白36(ZFP36)基因多态性的相关性。方法:以204例OSAHS患者为研究组,同时选取同期97例健康体检者作为对照组。通过TaqMan-PCR方法对2组的ZFP36位点(rs17879933、rs3746083、rs251864)进行检测,采用放射免疫法对TNF-α及其他生化指标进行检测,采用Monet32导系统监测记录所有入选者夜间睡眠呼吸相关指标。结果:研究组TNF-α、总胆固醇、血尿酸、舒张压、收缩压、BMI、腹围以及颈围均显著高于对照组(P<0.05)。研究组与对照组在ZFP36rs251864与rs17879933位点的基因型及等位基因频率分布差异有统计学意义(P<0.05)。rs251864GG及rs17879933Ⅱ基因型患者的腹围、BMI、TNF-α、三酰甘油(TG)水平均明显高于同一位点的其他2个基因型(P<0.05)。ZFP36的3个位点不同基因型间所有的睡眠呼吸监测指标均差异无统计学意义(P>0.05)。Logistic回归分析结果表明,在对性别、年龄等一系列因素予以控制后,未发现ZFP36的3个位点基因多态性与OSAHS之间存在相关性。结论:ZFP36可能是通过调节TNF-α等炎症因子及干预代谢参与OSAHS的发病进程,ZFP36的3个位点的突变不是OSAHS发生的独立危险因素。
Objective: To analyze the association between OSAHS and tumor necrosis factor (TNF) -α and zinc finger protein 36 (ZFP36) gene polymorphisms. Methods: A total of 204 OSAHS patients were selected as the research group, 97 healthy subjects were selected as the control group. The two groups of ZFP36 loci (rs17879933, rs3746083, rs251864) were detected by TaqMan-PCR method. The levels of TNF-α and other biochemical parameters were detected by radioimmunoassay. Monet32 guided monitoring system was used to record the correlation between nocturnal respiratory rate index. Results: The levels of TNF-α, total cholesterol, serum uric acid, diastolic blood pressure, systolic blood pressure, BMI, abdominal circumference and neck circumference of the study group were significantly higher than those of the control group (P <0.05). The genotype and allele frequency distribution of ZFP36rs251864 and rs17879933 in study group and control group were significantly different (P <0.05). The levels of abdominal circumference, BMI, TNF-α and triglyceride (TG) in rs251864GG and rs17879933Ⅱ genotypes were significantly higher than those in the other two genotypes (P <0.05). There was no significant difference in all sleep-respiration monitoring parameters among the three genotypes of ZFP36 (P> 0.05). Logistic regression analysis showed that there was no correlation between polymorphism of the three loci of ZFP36 and OSAHS after controlling a series of factors such as gender and age. Conclusion: ZFP36 may be involved in the pathogenesis of OSAHS by regulating the inflammatory factors such as TNF-α and its metabolism. The mutation of ZFP36 at 3 loci is not an independent risk factor for OSAHS.