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目的探讨Fractalkine(FKN)与慢性阻塞性肺疾病(COPD)并肺源性心脏病(简称肺心病)患者氧化应激状态的相关性及可能机制。方法 64例AECOPD住院患者按是否合并肺心病、是否使用乙酰半胱氨酸(NAC)、COPD严重程度以及心功能分为8组,8例志愿者为正常对照组,测定各组患者住院次日、治疗后第10天血清各项指标,并检查心脏彩超、肺功能、CAT评分。结果血清FKN、NF-κB、OX-LDL及hs CRP水平在AECOPD的各组患者中均较正常对照组升高(P<0.05),重症组及失代偿组升高明显(P<0.05),肺心病组治疗前及治疗后均高于COPD组(P<0.05),在COPD轻症干预组及肺心病代偿干预组治疗后下降明显(P<0.05),SOD则相反。FEV1在肺心病代偿干预组及COPD轻症干预组治疗后较治疗前升高(P<0.05)。肺动脉压在肺心病代偿干预组治疗前后有显著差异(P<0.05),肺心病失代偿组较代偿组明显升高(P<0.05),肺心病组与COPD组比较有显著差异(P<0.05)。CAT评分除在肺心病失代偿组外其它各组治疗前后均有显著差异(P<0.05),肺心病组与COPD组比较有统计学差异(P<0.05)。治疗前8组患者血清FKN与CAT评分及NF-κB、OX-LDL、hs CRP、肺动脉压呈正相关(r=0.417,0.521,0.401,0.456,0.395,P<0.05),与SOD负相关(r=-0.387,P<0.05),与FEV1无明显相关性(r=0.215,P>0.05)。结论 COPD并肺源性心脏病存在的氧化应激,与FKN密切相关,其机制可能系COPD持续低氧引起的氧化应激产物增多,激活NF-κB而促进FKN的生成和释放,NAC可能通过NF-κB途径降低FKN的生成,对早期肺心病的预防有一定作用。
Objective To investigate the correlation between the oxidative stress status of fractalkine (FKN) and chronic obstructive pulmonary disease (COPD) and patients with cor pulmonale (pulmonary heart disease) and its possible mechanism. Methods Sixty-four AECOPD inpatients were divided into 8 groups according to whether they had pulmonary heart disease, whether they used acetylcysteine (NAC), the severity of COPD and their cardiac function. Eight volunteers were normal control group, , The 10th day after treatment of serum indicators, and check the echocardiography, lung function, CAT score. Results Serum levels of FKN, NF-κB, OX-LDL and hs CRP in AECOPD group were significantly higher than those in control group (P <0.05), and were significantly higher in severe group and decompensated group (P <0.05) (P <0.05) before and after treatment in COPD group (P <0.05), and decreased significantly in COPD mild intervention group and compensatory cardiopulmonary intervention group (P <0.05), while SOD was the opposite. FEV1 increased after CPR intervention and COPD treatment (P <0.05). Pulmonary arterial pressure was significantly different between before and after treatment in decompensated pulmonary heart disease group (P <0.05), and decompensated pulmonary heart disease group was significantly higher than compensatory group (P <0.05), and pulmonary heart disease group and COPD group were significantly different P <0.05). CAT scores were significantly different (P <0.05) between other groups except COPD patients before and after treatment, and there was a significant difference between COPD group and COPD patients (P <0.05). There was a positive correlation between serum FKN and CAT score and NF-κB, OX-LDL, hs CRP and pulmonary artery pressure in the 8 groups before treatment (r = 0.417,0.521,0.401,0.456,0.395, P <0.05) = -0.387, P <0.05), but no significant correlation with FEV1 (r = 0.215, P> 0.05). Conclusions Oxidative stress in COPD with cor pulmonale is closely related to FKN. The possible mechanism is that the oxidative stress products induced by persistent hypoxia in COPD may increase, activate NF-κB and promote the production and release of FKN. NAC may pass NF-κB pathway to reduce the formation of FKN, early prevention of pulmonary heart disease have a role.