本文選題：支氣管哮喘　切入點(diǎn)：氣道重塑　出處：《山西醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:觀察間充質(zhì)干細(xì)胞(MSCs)對(duì)轉(zhuǎn)化生長因子-β1(TGF-β1)致上皮細(xì)胞-間質(zhì)轉(zhuǎn)化作用的影響,探討MSCs對(duì)哮喘氣道重塑的治療作用及可能的作用機(jī)制。方法:40只Wistar雄性大鼠分為四組:A.對(duì)照組、B.模型組、C.MSCs組、D.布地奈德組。除A組外,其余各組分別在第1、第8天采用10%卵白蛋白抗原混懸液1ml進(jìn)行腹腔注射致敏大鼠,第15天開始超聲霧化1%卵白蛋白激發(fā),20min/d,共8周;C組于第35、第45及第55天激發(fā)前30min尾靜脈注射臍帶MSCs 0.2ml(1×106個(gè)/ml);D組于每次激發(fā)前2h霧化吸入布地奈德2mg;A組以0.9%氯化鈉溶液代替卵白蛋白,其余干預(yù)方法同B組。在最后一次激發(fā)后的二十四小時(shí)之內(nèi),收集血清、支氣管肺泡灌洗液和肺組織,HE染色觀察氣道重塑病理改變,支氣管壁和平滑肌厚度由圖像分析軟件計(jì)算得出;支氣管肺泡灌洗液及血清中TGF-β1含量由酶聯(lián)免疫吸附試驗(yàn)檢測;肺組織E-鈣黏蛋白、α-平滑肌肌動(dòng)蛋白、纖維連接蛋白的表達(dá)由SABC法檢測。結(jié)果:B組大鼠支氣管壁及平滑肌厚度[(42.36±1.50、21.01±0.10)μm]顯著厚于A組[(25.69±0.27、14.97±0.13)μm];支氣管肺泡灌洗液及血清中TGF-β1含量[(21.01±0.18、70.97±0.23)μg/L]顯著高于A組[(1.14±0.19、23.05±0.16)μg/L];上皮標(biāo)志物E-鈣黏蛋白(0.256±0.087)表達(dá)顯著低于A組(0.469±0.012),間質(zhì)標(biāo)志物α-平滑肌肌動(dòng)蛋白、纖維連接蛋白[(0.521±0.030、0.527±0.022)]表達(dá)顯著高于A組[(0.371±0.007、0.387±0.020)](均P0.01)。C、D組大鼠支氣管壁及平滑肌厚度分別為32.40±2.50μm、35.86±0.55μm和15.71±0.89μm、18.72±0.89μm,支氣管肺泡灌洗液及血清中TGF-β1含量分別為3.53±0.43 ug/L、3.25±0.25 ug/L和31.07±0.89 ug/L、32.08±0.18 ug/L,均顯著低于B組(均P0.01);E-鈣黏蛋白表達(dá)[(0.308±0.023)、(0.296±0.010)]顯著高于B組,α-平滑肌肌動(dòng)蛋白和纖維連接蛋白表達(dá)[(0.438±0.057)、(0.445±0.027)和(0.459±0.041)、(0.458±0.029)]顯著低于B組(均P0.01)。結(jié)論:1、TGF-β1誘導(dǎo)的上皮細(xì)胞-間質(zhì)轉(zhuǎn)化是哮喘氣道重塑的機(jī)制之一;2、MSCs通過抑制TGF-β1誘導(dǎo)的上皮細(xì)胞-間質(zhì)轉(zhuǎn)化,對(duì)支氣管哮喘氣道重塑發(fā)揮治療作用。
[Abstract]:Aim: to observe the effect of mesenchymal stem cells (MSCs) on epithelial cell-mesenchymal transformation induced by transforming growth factor- 尾 _ 1- TGF- 尾 _ 1 (TGF- 尾 _ 1). To investigate the therapeutic effect and possible mechanism of MSCs on airway remodeling in asthmatic rats, 40 Wistar male rats were divided into four groups: control group, control group, C.MSCs group, D 路budesonide group, with the exception of group A. The other groups were sensitized by intraperitoneal injection of 10% ovalbumin antigen suspension (1ml) on the 1st and 8th day, respectively. On the 15th day, 1% ovalbumin was stimulated by ultrasound for 20 min / d. After 8 weeks, 30min caudal vein injection of MSCs 0.2ml(1 脳 106 / ml / d was performed in group C at 35th, 45th and 55th day. Group D inhaled budesonide 2 mg / g of budesonide and inhaled 2 mg of budesonide with 0.9% sodium chloride 2 h before stimulation. Instead of ovalbumin, The other intervention methods were the same as group B. within 24 hours after the last stimulation, the serum, bronchoalveolar lavage fluid and lung tissue were collected to observe the pathological changes of airway remodeling. The thickness of bronchial wall and smooth muscle was calculated by image analysis software; the content of TGF- 尾 1 in bronchoalveolar lavage fluid and serum was measured by enzyme linked immunosorbent assay (Elisa); Results the thickness of bronchial wall and smooth muscle in group B was significantly thicker than that in group A [25.69 鹵0.270.97 鹵0.13 渭 m], and the content of TGF- 尾 _ 1 in bronchoalveolar lavage fluid and serum [21.01 鹵0.1870.97 鹵0.23 渭 g / L] was significantly higher than that in group A [1.14 鹵0.19 鹵23.05 鹵0.16 渭 g / L]. The expression of 偽 -smooth muscle actin was significantly lower in group A than in group A (0.256 鹵0.087), and the expression of 偽 -smooth muscle actin was significantly lower than that in group A (0.469 鹵0.012). The expression of fibronectin [0.521 鹵0.030 鹵0.527 鹵0.022] was significantly higher than that in group A [0.371 鹵0.007 鹵0.387 鹵0.020] (the thickness of bronchial wall and smooth muscle in group A was 32.40 鹵2.50 渭 m, 35.86 鹵0.55 渭 m and 15.71 鹵0.89 渭 m, 18.72 鹵0.89 渭 m, respectively). The levels of TGF- 尾 _ 1 in bronchoalveolar lavage fluid and serum were 3.53 鹵0.43 渭 L ~ 3.25 鹵0.25 ug/L and 31.07 鹵0.89 鹵0.89 渭 m, respectively, which were significantly lower than those in group B (P < 0.05). The expressions of 偽 -smooth muscle actin and fibronectin [0.438 鹵0.0577.45 鹵0.027] and 0.459 鹵0.041 (0.458 鹵0.029) were significantly lower in group B than those in group B (all P 0.01). Conclusion the expression of 偽 -smooth muscle actin and fibronectin is the mechanism of airway remodeling in asthma. Mesenchymal mesenchymal transformation induced by TGF- 尾 1 was inhibited by TGF- 尾 1. To play a therapeutic role in bronchial asthma airway remodeling.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R562.25

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本文編號(hào)：1675623