中华内科杂志
中華內科雜誌
중화내과잡지
CHINESE JOURNAL OF INTERNAL MEDICINE
2012年
11期
863-866
,共4页
佘惟槟%刘先胜%倪望%陈仕新%徐永健
佘惟檳%劉先勝%倪望%陳仕新%徐永健
사유빈%류선성%예망%진사신%서영건
肺疾病,慢性阻塞性%巨噬细胞迁移抑制因子%吸烟
肺疾病,慢性阻塞性%巨噬細胞遷移抑製因子%吸煙
폐질병,만성조새성%거서세포천이억제인자%흡연
Pulmonary disease,chronic obstructive%Macrophage migration inhibitory factor%Smoking
目的 通过检测吸烟患或未患慢性阻塞性肺疾病(COPD)患者肺组织中巨噬细胞移动抑制因子(MIF)表达水平,为进一步了解COPD易患机制提供基础研究资料.方法 肺组织来源于因肺癌行肺叶切除术的41例患者,分吸烟患COPD组(16例)、吸烟未患COPD组(13例)、无吸烟对照组(12例)3组.所有受试者均于术前1周做肺功能检查[第1秒用力呼气容积(FEV1),用力肺活量(FVC)],采用实时定量PCR和免疫组化检测肺组织中MIF mRNA和蛋白表达水平,并行相关分析.结果 (1)实时定量PCR检测肺组织内MIF mRNA表达水平,吸烟患COPD组(4.87±1.79)高于吸烟未患COPD组(2.16±0.72),而吸烟未患COPD组又高于无吸烟对照组(1.09 ±0.48;P＜0.01).(2)免疫组化显示,肺组织内MIF蛋白表达吸光度值吸烟患COPD组(0.277±0.025)高于吸烟未患COPD组(0.199 ±0.034),而吸烟未患COPD组高于无吸烟对照组(0.130 ±0.021；P ＜0.01).(3)相关性分析:肺组织内MIF mRNA表达与FEV1占预计值百分比、FEV1/FVC呈负相关(r分别为-0.578、-0.607,P值均＜0.01).结论 吸娴患COPD者肺组织中MIF表达明显增加,且与气流受限程度呈正相关,提示MIF可能在吸烟致COPD发病机制中起重要作用.
目的 通過檢測吸煙患或未患慢性阻塞性肺疾病(COPD)患者肺組織中巨噬細胞移動抑製因子(MIF)錶達水平,為進一步瞭解COPD易患機製提供基礎研究資料.方法 肺組織來源于因肺癌行肺葉切除術的41例患者,分吸煙患COPD組(16例)、吸煙未患COPD組(13例)、無吸煙對照組(12例)3組.所有受試者均于術前1週做肺功能檢查[第1秒用力呼氣容積(FEV1),用力肺活量(FVC)],採用實時定量PCR和免疫組化檢測肺組織中MIF mRNA和蛋白錶達水平,併行相關分析.結果 (1)實時定量PCR檢測肺組織內MIF mRNA錶達水平,吸煙患COPD組(4.87±1.79)高于吸煙未患COPD組(2.16±0.72),而吸煙未患COPD組又高于無吸煙對照組(1.09 ±0.48;P＜0.01).(2)免疫組化顯示,肺組織內MIF蛋白錶達吸光度值吸煙患COPD組(0.277±0.025)高于吸煙未患COPD組(0.199 ±0.034),而吸煙未患COPD組高于無吸煙對照組(0.130 ±0.021；P ＜0.01).(3)相關性分析:肺組織內MIF mRNA錶達與FEV1佔預計值百分比、FEV1/FVC呈負相關(r分彆為-0.578、-0.607,P值均＜0.01).結論 吸嫻患COPD者肺組織中MIF錶達明顯增加,且與氣流受限程度呈正相關,提示MIF可能在吸煙緻COPD髮病機製中起重要作用.
목적 통과검측흡연환혹미환만성조새성폐질병(COPD)환자폐조직중거서세포이동억제인자(MIF)표체수평,위진일보료해COPD역환궤제제공기출연구자료.방법 폐조직래원우인폐암행폐협절제술적41례환자,분흡연환COPD조(16례)、흡연미환COPD조(13례)、무흡연대조조(12례)3조.소유수시자균우술전1주주폐공능검사[제1초용력호기용적(FEV1),용력폐활량(FVC)],채용실시정량PCR화면역조화검측폐조직중MIF mRNA화단백표체수평,병행상관분석.결과 (1)실시정량PCR검측폐조직내MIF mRNA표체수평,흡연환COPD조(4.87±1.79)고우흡연미환COPD조(2.16±0.72),이흡연미환COPD조우고우무흡연대조조(1.09 ±0.48;P＜0.01).(2)면역조화현시,폐조직내MIF단백표체흡광도치흡연환COPD조(0.277±0.025)고우흡연미환COPD조(0.199 ±0.034),이흡연미환COPD조고우무흡연대조조(0.130 ±0.021；P ＜0.01).(3)상관성분석:폐조직내MIF mRNA표체여FEV1점예계치백분비、FEV1/FVC정부상관(r분별위-0.578、-0.607,P치균＜0.01).결론 흡한환COPD자폐조직중MIF표체명현증가,차여기류수한정도정정상관,제시MIF가능재흡연치COPD발병궤제중기중요작용.
Objective To investigate the expression of macrophage migration inhibition factor (MIF) in pulmonary tissues of the smokers with and without chronic obstructive pulmonary disease (COPD).Methods The subjects were assigned into three groups:non-smokers without COPD (control group,n =12),smokers without COPD (smoker group,n =13) and smokers with COPD (COPD group,n =16).The specimens were obtained from lung tissues as far away from cancer focus as possible (＞ 5cm).Real-time quantitative PCR and immunohistochemistry were used to investigate the expression and distribution of MIF in pulmonary tissues.The relationship between the severity of airflow obstruction and the differential expressions of MIF in lung tissues of the smokers with or without COPD was analyzed.Results (1) MIF mRNA expression in COPD group (4.87 ± 1.79) was higher than that in the smoker group (2.16 ±0.72;P＜0.01),which was higher than that in the control group (1.09 ±0.48;P ＜0.01).(2)Immunohistochemistry analysis showed that MIF protein expression in lung tissues of the COPD group (0.277±0.025) was higher than that in the smokers group (0.199 ±0.034;P ＜0.01),which was significantly higher than that in control group (0.130 ±0.021 ;P ＜0.01).(3) Correlation analysis of MIF mRNA expression in the lung tissues and pulmonary function parameters of forced expired volume in one second (FEV1) percentage of predicted (FEV1 pred) and ratio of FEV1 to forced vital capacity (FEV1/FVC) suggested that MIF mRNA expression in the lung tissues was negatively related with FEV1 pred (r=-0.578,P ＜ 0.01) and FEV1/FVC (r =-0.607,P ＜ 0.01).Conclusions MIF expression significantly increases in the smokers with COPD,and MIF level in the lung is positively correlated with airflow limitation.The results suggest that MIF may play an important role in the pathogenesis of smokinginduced COPD.
