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N-乙酰半胱氨酸对慢性肺心病患者肺纤维化、内皮损伤及血管活性因子的影响 被引量:5

Effect of N-acetylcysteine on pulmonary fibrosis,endothelial injury and vasoactive factors in patients with chronic pulmonary heart disease
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摘要 目的:研究N-乙酰半胱氨酸对慢性肺心病患者肺纤维化、内皮损伤及血管活性因子的影响。方法:选择在本医院收治的COPD合并慢性肺心病患者并随机分为两组,NAC组接受N-乙酰半胱氨酸联合常规治疗,对照组接受常规治疗。治疗前后检测血清中肺纤维化指标、内皮损伤氧化应激损伤指标及血管活性因子的含量。结果:治疗后14、28天时,两组血清中TGF-β1、β-catenin、uPA、MMP7、ET-1、VEGF、IMD、ADM、MDA、8-iso-PGF2α、AOPP的含量较治疗前显著降低且NAC组血清中TGF-β1、β-catenin、uPA、MMP7、ET-1、VEGF、IMD、ADM、MDA、8-iso-PGF2α、AOPP的含量显著低于对照组。结论:N-乙酰半胱氨酸对慢性肺心病患者肺纤维化、内皮损伤及血管活性因子的分泌具有显著抑制作用。 Objective:To study the effect of N-acetylcysteine on pulmonary fibrosis,endothelial injury and vasoactive factors in patients with chronic pulmonary heart disease.Methods:Patients with COPD complicated by chronic pulmonary heart disease who were treated in Zigong Third People's Hospital between October 2015 and December 2016 were selected and randomly divided into two groups,NAC group received N-acetylcysteine combined with conventional therapy,and the control group received conventional therapy.Serum levels of pulmonary fibrosis indexes,endothelial injury and oxidative stress injury indexes and vasoactive factors were measured before and after treatment.Results:Fourteen days and 28 dafter treatment,serum TGF-β1,β-catenin,uPA,MMP7,ET-1,VEGF,IMD,ADM,MDA,8-iso-PGF2αand AOPP levels of both groups of patients were significantly lower than those before treatment and serum TGF-β1,β-catenin,uPA,MMP7,ET-1,VEGF,IMD,ADM,MDA,8-iso-PGF2αand AOPP levels of NAC group were significantly lower than those of control group.Conclusions:N-acetylcysteine can significantly inhibit pulmonary fibrosis,endothelial injury and vasoactive factor secretion in patients with chronic pulmonary heart disease.
作者 陈其苹 CHEN Qi-ping(Respiratory Medicine Department, Zigong Third People's Hospital in Sichuan Province, Zigong 643020, Chin)
出处 《海南医学院学报》 CAS 2017年第12期1616-1619,共4页 Journal of Hainan Medical University
基金 四川省教育厅资助项目(15zb068)~~
关键词 肺源性心脏病 N-乙酰半胱氨酸 肺纤维化 内皮损伤 Pulmonary heart disease N-acetylcysteine Pulmonary fibrosis Endothelial injury
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