慢性阻塞性肺疾病患者的血浆晚期糖基化终产物和皮肤自发荧光增加。
Plasma advanced glycation end-products and skin autofluorescence are increased in COPD.
机构信息
Maastricht University Medical Center+ (MUMC), Maastricht.
出版信息
Eur Respir J. 2014 Feb;43(2):430-8. doi: 10.1183/09031936.00135312. Epub 2013 May 3.
Chronic obstructive pulmonary disease (COPD) is associated with systemic inflammation and oxidative stress. These conditions may lead to the formation of advanced glycation end-products (AGEs). In this study we investigated in 88 COPD patients and 55 control subjects (80% ex-smokers) the association of the plasma protein-bound AGEs N(ε)-(carboxymethyl)lysine (CML), pentosidine, N(ε)-(carboxyethyl)lysine (CEL), and AGE accumulation in skin by skin autofluorescence (AFR), with lung function. Mean ± sd plasma CML was decreased (COPD 61.6 ± 15.6 nmol · mmol(-1) lysine, never-smokers 80.7 ± 19.8 nmol · mmol(-1) lysine and ex-smokers 82.9 ± 19.3 nmol · mmol(-1) lysine) and CEL (COPD 39.1 ± 10.9 nmol · mmol(-1) lysine, never-smokers 30.4 ± 5.0 nmol · mmol(-1) lysine and ex-smokers 27.7 ± 6.4 nmol · mmol(-1) lysine) and AFR (COPD 3.33 ± 0.67 arbitrary units (AU), never-smokers 2.24 ± 0.45 AU and ex-smokers 2.31 ± 0.47 AU) were increased in COPD patients compared to controls. Disease state was inversely associated with CML, and linearly associated with CEL and AFR. Performing regression analyses in the total group, CEL and AFR showed a negative association and CML a positive association with lung function, even after correction for potential confounders. In conclusion, CEL and AFR were negatively and CML was positively associated with disease state. In the total group only the AGEs showed an association with forced expiratory volume in 1 s. Our data suggest that AGEs are involved in the pathophysiology of COPD, although their exact role remains to be determined.
慢性阻塞性肺疾病（COPD）与全身炎症和氧化应激有关。这些情况可能导致晚期糖基化终产物（AGEs）的形成。在这项研究中，我们调查了 88 名 COPD 患者和 55 名对照受试者（80%为戒烟者），血浆蛋白结合的 AGEs N（ε）-（羧甲基）赖氨酸（CML）、戊糖素、N（ε）-（羧乙基）赖氨酸（CEL）与皮肤 AGE 积累（通过皮肤自发荧光（AFR））与肺功能的关系。平均±标准差血浆 CML 降低（COPD 61.6±15.6nmol·mmol（-1）赖氨酸，从不吸烟者 80.7±19.8nmol·mmol（-1）赖氨酸和戒烟者 82.9±19.3nmol·mmol（-1）赖氨酸）和 CEL（COPD 39.1±10.9nmol·mmol（-1）赖氨酸，从不吸烟者 30.4±5.0nmol·mmol（-1）赖氨酸和戒烟者 27.7±6.4nmol·mmol（-1）赖氨酸）和 AFR（COPD 3.33±0.67 任意单位（AU），从不吸烟者 2.24±0.45 AU 和戒烟者 2.31±0.47 AU）在 COPD 患者中高于对照组。疾病状态与 CML 呈负相关，与 CEL 和 AFR 呈线性相关。在总组中进行回归分析时，CEL 和 AFR 与肺功能呈负相关，而 CML 与肺功能呈正相关，即使在纠正潜在混杂因素后也是如此。总之，CEL 和 AFR 与疾病状态呈负相关，而 CML 则呈正相关。在总组中，只有 AGEs 与 1 秒用力呼气量（FEV1）呈正相关。我们的数据表明，AGEs 参与了 COPD 的病理生理学，但它们的确切作用仍有待确定。
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