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辛伐他汀对COPD患者肺功能、血清IL—17、IL—13及脂联素的影响(1)
http://www.100md.com 2012年9月15日 郭新跃
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     [摘要] 目的 探讨辛伐他汀对慢性阻塞性肺疾病(COPD)患者的肺功能、血清IL—17、IL—13及脂联素的影响。 方法 对照组采用常规治疗,治疗组在此基础上加辛伐他汀,观察两组治疗前后肺功能、血清IL—17、IL—13及脂联素变化情况。 结果 COPD患者组血清IL—17、IL—13水平较健康组显著升高(P < 0.01);而FEV1%、FEVl/ FVC及脂联素水平则显著降低(P < 0.01);治疗组治疗后血清IL—17、IL—13较治疗前显著降低,FEV1%、FEVl/ FVC及脂联素水平则显著升高(均P < 0.01);治疗后组间比较,血清IL—17、IL—13、脂联素、FEV1%及FEVl/ FVC差异也有统计学意义(均P < 0.05);炎症介质IL—17、IL—13和脂联素的含量与患者FEV1%、FFEVl/FVC均显著相关。 结论 辛伐他汀治疗能改善COPD患者肺功能,升高脂联素水平并降低IL—17、IL—13水平,辛伐他汀对COPD的治疗机制可能与抑制炎症介质有关。

    [关键词] 辛伐他汀;慢性阻塞性肺疾病;肺功能;白介素17;白介素13;脂联素

    [中图分类号] R563.8 [文献标识码] B [文章编号] 1673—9701(2012)26—0061—03

    Influnce of Simvastatin on lung function and serum IL—17,IL—13, adiponectin in patients with chronic obstructive pulmonary diseases

    GUO Xinyue

    Department of Respiratory Medicine, Yuanjiang City People's Hospital, Hunan Province, YuanJiang 413000, China

    [Abstract] Objective To explore the influence of lung function and serum IL—17, IL—13, adiponectin treated by Simvastatin on COPD patients. Methods The control group was treated only with conventional therapy, and the treatment group was given Simvastatin besides conventional therapy. Observed the change of lung function and serum IL—17, IL—13, adiponectin before and after treated in the two groups. Results The serum IL—17, IL—13 levels of COPD group were higher than the healthy control group(P < 0.01), while the levels of FEV1%,FEVl/FVC and adiponectin was converse; The nerve levels of IL—17, IL—13 after Simvastatin treatment were significant lower than before treatment in the treatment group, FEV1% and FEVl/FVC and adiponectin were significant higher than before treatment (all P < 0.01); The serum level of IL—17, IL—13, adiponectin were significant correlation with FEV1%, FEVl/FVC in patients with COPD. Conclusion Simvastatin treatment can improve the lung function, adiponectin levels, and reduce the IL—17, IL—13 levels in patients with COPD, the mechanism of simvastatin in treatment of COPD may have relevant with inhibit mediators of inflammation ......

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