CAJ | 학술논문

目的初步分析慢性阻塞性肺疾病(COPD)患者外周骨骼肌萎缩蛋白质组.方法研究对象为2010年2-7月昆明医学院第一附属医院收治的16例COPD患者(COPD组)和同期收治的年龄匹配的8例骨折患者(对照组).根据患者体质指数(BMI)、去脂肪指数、股四头肌的周径、股四头肌最大主动收缩力结果,COPD组又分为:(1)骨骼肌萎缩组8例:男6例,女2例；平均(70±8)岁；(2)骨骼肌非萎缩组8例:男5例,女3例；平均(74±8)岁.对照组男6例,女2例；平均(72±6)岁.利用二维凝胶电泳分离出各组受试者股四头肌外侧肌组织的总蛋白；通过PDQuest图像软件比较电泳图谱中的异常蛋白点,识别差异表达蛋白；应用质谱仪得到相应的肽质量指纹谱；然后搜索数据库鉴定部分差异蛋白点.结果获得分辨率和重复性均较好的双向凝胶电泳图谱,并鉴定出可能与COPD肌萎缩发生密切相关的12种蛋白,其中8种结构蛋白(心肌α-肌动蛋白解离亚型c、心肌肌球蛋白调节轻链-2、肌红蛋白及其亚型、心肌β-肌球蛋白解离亚型7c多肽、骨骼肌α-肌动蛋白、心肌α-肌动蛋白解离亚型b、血红蛋白珠蛋白1α链、肌球蛋白轻链-6B),4种功能蛋白(烯醇化酶1-A链、慢骨骼肌肌钙蛋白T1解离亚型a、碳酸酐酶、慢骨骼肌肌钙蛋白T解离亚型b).结论 COPD患者常并发有明显外周骨骼肌萎缩,原因可能与外周骨骼肌结构蛋白和功能蛋白数量及质量的改变有关.
목적 초보분석만성조새성폐질병(COPD)환자외주골격기위축단백질조.방법 연구대상위2010년2-7월곤명의학원제일부속의원수치적16례COPD환자(COPD조)화동기수치적년령필배적8례골절환자(대조조).근거환자체질지수(BMI)、거지방지수、고사두기적주경、고사두기최대주동수축력결과,COPD조우분위:(1)골격기위축조8례:남6례,녀2례；평균(70±8)세；(2)골격기비위축조8례:남5례,녀3례；평균(74±8)세.대조조남6례,녀2례；평균(72±6)세.이용이유응효전영분리출각조수시자고사두기외측기조직적총단백；통과PDQuest도상연건비교전영도보중적이상단백점,식별차이표체단백；응용질보의득도상응적태질량지문보；연후수색수거고감정부분차이단백점.결과 획득분변솔화중복성균교호적쌍향응효전영도보,병감정출가능여COPD기위축발생밀절상관적12충단백,기중8충결구단백(심기α-기동단백해리아형c、심기기구단백조절경련-2、기홍단백급기아형、심기β-기구단백해리아형7c다태、골격기α-기동단백、심기α-기동단백해리아형b、혈홍단백주단백1α련、기구단백경련-6B),4충공능단백(희순화매1-A련、만골격기기개단백T1해리아형a、탄산항매、만골격기기개단백T해리아형b).결론 COPD환자상병발유명현외주골격기위축,원인가능여외주골격기결구단백화공능단백수량급질량적개변유관.
Objective To conduct a preliminary proteomic study of chronic obstructive pulmonary disease (COPD) with peripheral skeletal muscle atrophy.Methods A total of 16 COPD patients and 8 aged-matched persons because of bone fractures were recruited in First Hospital Affiliated to Kunming Medical College from February to July in 2010. According to body mass index,fat free mass index,quadriceps femoris perimeter and quadriceps femoris active contraction,they were divided into those with muscle atrophy (group A,n=8) and those without (group B,n=8).There were 6 males and 2 females with an average age of (70±8) years in the group A and 5 males and 3 females with an average age of (74±8) years in the group B. And the control group had 6 males and 2 females with an average age of (72±6) years.All samples of total quadriceps protein were separated by two-dimensional gel electrophoresis.The abnormal protein points on electrophoresis were compared by PDQuest image software.And the differential protein expression was detected. Then the corresponding peptide quality fingerprint spectrum was analyzed by mass spectrometer.Finally the differential protein points were partially detected by a search of database.Results The two-dimensional gel electrphoresis yielded an excellent profile of resolution and repeatability.And 12 proteins likely to cause skeletal muscle atrophy in COPD were identified.Among them,8 proteins belonged to structural proteins (actin alpha cardiac muscle isoform CRA_c,myosin regulatory light chain 2,ventricular/cardiac muscle isoform,myoglobin isoform myosin heavy polypeptide 7 cardiac muscle beta isoform CRA_c,actin,alpha skeletal muscle,actin alpha cardiac muscle isoform CRA_b,hemoglobin alpha 1 globin chain & myosin light chain 6B) and 4 proteins were of functional proteins (chain A,crystal structure of human enolase ; troponin T,slow skeletal muscle isoform alpha,carbonate anhydrase,troponin T & slow skeletal muscle isoform b).Conclusions COPD patients are often accompanied with obvious peripheral skeletal muscle atrophy. It may be caused by quantitative or qualitative changes of peripheral skeletal structural and functional proteins.