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衰老和吸烟导致血浆表面活性剂蛋白和蛋白酶失衡,并与气道阻塞相关。

Ageing and smoking contribute to plasma surfactant proteins and protease imbalance with correlations to airway obstruction.

机构信息

Department of Medicine, Division of Pulmonary Medicine, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.

出版信息

BMC Pulm Med. 2011 Apr 19;11:19. doi: 10.1186/1471-2466-11-19.

Abstract

BACKGROUND

A significant number of young people start smoking at an age of 13-15, which means that serious smoking-evoked changes may have been occurred by their twenties. Surfactant proteins (SP) and matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) have been linked to cigarette smoke induced lung remodelling and chronic obstructive pulmonary disease (COPD). However, the level of these proteins has not been examined during ageing or in young individuals with short smoking histories.

METHODS

Plasma levels of SP-A, SP-D, MMP-9, and TIMP-1 were measured by EIA/ELISA from young (18-23 years) non-smoking controls (YNS) (n = 36), smokers (YS) (n = 51), middle aged/elderly (37-77 years) non-smoking controls (ONS) (n = 40), smokers (OS) (n = 64) (FEV1/FVC >0.7 in all subjects) and patients with COPD (n = 44, 35-79 years).

RESULTS

Plasma levels of SP-A increased with age and in the older group in relation to smoking and COPD. Plasma SP-D and MMP-9 levels did not change with age but were elevated in OS and COPD as compared to ONS. The TIMP-1 level declined with age but increased in chronic smokers when compared to ONS. The clearest correlations could be detected between plasma SP-A vs. age, pack years and FEV1/FVC. The receiver operating characteristic (ROC) curve analysis revealed SP-A to be the best marker for discriminating between patients with COPD and the controls (area under ROC curve of 0.842; 95% confidence interval, 0.785-0.899; p < 0.001).

CONCLUSIONS

Age has a significant contribution to potential markers related to smoking and COPD; SP-A seems to be the best factor in differentiating COPD from the controls.

摘要

背景

相当数量的年轻人在 13-15 岁时开始吸烟,这意味着到 20 多岁时,严重的吸烟引起的变化可能已经发生。表面活性剂蛋白(SP)和基质金属蛋白酶(MMP)及其组织抑制剂(TIMP)与香烟烟雾引起的肺重塑和慢性阻塞性肺疾病(COPD)有关。然而,在衰老过程中或在吸烟史较短的年轻人中,这些蛋白质的水平尚未得到检查。

方法

通过 EIA/ELISA 从年轻(18-23 岁)非吸烟对照(YNS)(n = 36)、吸烟者(YS)(n = 51)、中年/老年(37-77 岁)非吸烟对照(ONS)(n = 40)、吸烟者(OS)(n = 64)(所有受试者 FEV1/FVC >0.7)和 COPD 患者(n = 44,35-79 岁)中测量 SP-A、SP-D、MMP-9 和 TIMP-1 的血浆水平。

结果

SP-A 的血浆水平随年龄增长,在老年组中与吸烟和 COPD 有关。SP-D 和 MMP-9 的血浆水平与年龄无关,但在 OS 和 COPD 中与 ONS 相比升高。TIMP-1 水平随年龄下降,但与 ONS 相比,慢性吸烟者的水平升高。可以在血浆 SP-A 与年龄、包年和 FEV1/FVC 之间检测到最清晰的相关性。受试者工作特征(ROC)曲线分析显示 SP-A 是区分 COPD 患者和对照组的最佳标志物(ROC 曲线下面积为 0.842;95%置信区间,0.785-0.899;p <0.001)。

结论

年龄对与吸烟和 COPD 相关的潜在标志物有重要贡献;SP-A 似乎是区分 COPD 与对照组的最佳因素。

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