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作 者:何大川[1,2] 傅炜萍[1] 龙翔宇[1] 方利洲[1] 戴路明[1]
机构地区:[1]昆明医学院第一附属医院呼吸科,昆明650031 [2]四川省南充市中心医院,637000
出 处:《重庆医学》2011年第35期3537-3539,3542,共4页Chongqing medicine
基 金:云南省科技计划资助项目(2008CD011)
摘 要:目的探讨慢性阻塞性肺疾病(COPD)骨骼肌萎缩患者股外侧肌过氧化酶体增殖物激活受体α(PPARα)mRNA表达和血清炎症因子水平。方法将COPD患者分为COPD萎缩组、COPD非萎缩组,10例健康体检者作为对照组。检查患者及对照组用力呼气肺活量(FVC)、第一秒用力呼气量占预计值的百分比(FEV1%PRE)及第一秒用力呼气量占用力肺活量百分比(FEV1%FVC)。采用酶联免疫吸附测定(ELISA)试剂盒检测患者血清肿瘤坏死因子α(TNF-α)、白细胞介素-8(IL-8)水平,实时荧光定量PCR检测患者股外侧肌PPARαmRNA表达水平。结果与COPD非萎缩组及对照组比较,COPD萎缩组患者股外侧肌PPARαmRNA表达下调(P<0.01),PPARαmRNA表达与FEV1%PRE及FEV1%FVC呈正相关(r=0.574、r=0.613,P<0.01),与TNF-α及IL-8呈负相关(r=-0.618、r=-0.690,P<0.01)。结论 PPARαmRNA表达的下调与COPD全身炎症反应及肺功能下降相关,在COPD骨骼肌萎缩中有着重要作用。Objective To explore the expression levels of peroxisome proliferator-activated receptor alpha(PPARα) mRNA in vastus lateralis muscle and serum inflammatory factors of patients with chronic obstructive pulmonary disease(COPD) accompanied by skeletal muscle atrophy.Methods Patients with COPD were divided into COPD atrophy group and COPD non-atrophy group.10 healthy people who had undergone physical examination served as control group.Forced vital capacity(FVC),percentage of forced expiratory volume in first second to prediction(FEV1%PRE) and percentage of forced expiratory volume in first second to forced vital capacity(FEV1%FVC) of patients and healthy people were examined.Enzyme-linked immunosorbent assay(ELISA) kit was employed to assay serum levels of tumor necrosis factor alpha(TNF-α) and interleukin(IL)-8.Real-time fluorescent quantitative PCR was used to detect the expression level of PPARα mRNA in vastus lateralis muscle of patients.Results The mRNA expression of PPARα in vastus lateralis muscle of patients in COPD atrophy group decreased when compared to that in COPD non-atrophy group and control group(P0.01).It had positive correlation with FEV1%PRE and FEV1%FVC(r=0.574,r=0.613,P0.01) and negative correlation with TNF-α and IL-8(r=-0.618,r=-0.690,P0.01).Conclusion Down-regulation of PPARα mRNA expression which has an important role in skeletal muscle atrophy is related to systemic inflammation and decline of pulmonary function.
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