本文選題：慢性阻塞性肺疾病 + 過氧化物酶體增殖因子活化受體γ　； 參考：《中國老年學(xué)雜志》2017年10期

【摘要】：目的研究過氧化物酶體增殖因子活化受體(PPAR)γ在大鼠慢性阻塞性肺疾病(COPD)模型中的表達(dá)及意義。方法 SD大鼠24只,隨機(jī)分為對照組(A組)和實驗5 w組(B組)和實驗10 w組(C組),每組8只。實驗組采用氣管內(nèi)注入胰蛋白酶和熏香煙的方法,建立大鼠COPD模型。從開始實驗起,實驗第5周處死實驗B組;第10周處死C組。應(yīng)用病理學(xué)及肺功能檢查評價COPD動物模型,免疫組化RT-PCR和Western印跡方法檢測大鼠肺組織PPARγmRNA及蛋白的表達(dá)水平。結(jié)果 B組與A組比較,炎癥反應(yīng)明顯,已形成慢性阻塞性肺氣腫,并于第10周形成明顯的肺氣腫。PPARγ在正常肺組織與患慢性阻塞性肺氣腫的肺組織均有表達(dá),主要定位在炎性浸潤細(xì)胞的核和核周圍區(qū),比較大鼠肺組織PPARγ在COPD中的表達(dá)(吸光度值A(chǔ)值):A組為0.497±0.078,B組PPARγ在肺組織中表達(dá)減弱(0.329±0.024),C組PPARγ在肺組織中表達(dá)明顯減弱(0.216±0.049),差異均有統(tǒng)計學(xué)意義(P0.01)。PPARγmRNA表達(dá)隨著COPD病程的進(jìn)展逐漸降低,A組光密度比值為(1.06±0.10);B組為(0.50±0.02);C組為(0.27±0.02),與A組比較,B、C組差異有統(tǒng)計學(xué)意義(均P0.01)。Western印跡也表明COPD模型B組和C組比A組PPARγ蛋白表達(dá)降低,且B組蛋白表達(dá)降低的更為明顯。結(jié)論 PPARγ在COPD的發(fā)生及進(jìn)展中起重要作用,并且隨著病程的發(fā)展,蛋白表達(dá)降低更為顯著,因此該蛋白有望成為未來COPD治療的新靶點。
[Abstract]:Objective to study the expression and significance of peroxisome proliferating factor-activated receptor (PPAR) 緯 in rat chronic obstructive pulmonary disease (COPD) model. Methods Twenty-four Sprague-Dawley rats were randomly divided into three groups: control group (group A), experimental group (group B) for 5 weeks and experimental group for 10 weeks (group C) with 8 rats in each group. Rat COPD model was established by intratracheal injection of trypsin and smoked cigarette. From the beginning of the experiment, group B was killed at the 5th week and group C was killed at the 10th week. The expression of PPAR 緯 mRNA and protein in rat lung tissue was detected by immunohistochemistry RT-PCR and Western blot. Results compared with group A, the inflammatory reaction in group B was obvious and the chronic obstructive emphysema had been formed, and the expression of PPAR 緯 in both normal lung tissues and lung tissues with chronic obstructive emphysema was observed at the 10th week. Mainly located in the nucleus and peri-nucleus of inflammatory infiltrating cells, The expression of PPAR 緯 in lung tissue of rats was significantly decreased (0.216 鹵0.049) in group B (0.329 鹵0.024) and group C (0.329 鹵0.024). The difference was statistically significant (P0.01) .PPAR 緯 mRNA expression with the progression of COPD. The ratio of optical density in group A was (1.06 鹵0.10) and (0.50 鹵0.02) in group B was (0.27 鹵0.02), which was significantly lower than that in group A (P0.01). Western blotting also showed that the expression of PPAR 緯 protein in group B and C was lower than that in group A. Moreover, the expression of B-histone decreased more obviously. Conclusion PPAR 緯 plays an important role in the pathogenesis and progression of COPD, and with the development of the course of disease, the expression of PPAR 緯 protein decreases more significantly. Therefore, PPAR 緯 may become a new target for the treatment of COPD in the future.
【作者單位】： 首都醫(yī)科大學(xué)附屬北京世紀(jì)壇醫(yī)院變態(tài)反應(yīng)科;首都醫(yī)科大學(xué)附屬北京胸科醫(yī)院重癥監(jiān)護(hù)室;北京大學(xué)醫(yī)學(xué)部生物化學(xué)與分子生物學(xué)系;內(nèi)蒙古電力中心醫(yī)院包頭醫(yī)學(xué)院第二附屬醫(yī)院;
【分類號】：R-332;R563.9

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