【摘要】：目的研究煙草煙霧暴露對支氣管哮喘（簡稱哮喘）大鼠氣道CCR6(Chemokinereceptor6)表達的影響，探討吸煙誘發(fā)和加重哮喘氣道炎癥的免疫學(xué)機制。 方法雄性Wistar大鼠40只，隨機分為對照組、煙霧暴露組、哮喘組和哮喘+煙霧暴露組，每組各10只。建立哮喘大鼠模型和哮喘大鼠煙草煙霧暴露模型，采集大鼠支氣管肺泡灌洗液(BALF)行白細胞計數(shù)及細胞分類，蘇木精-伊紅（HE）染色觀察肺組織病理學(xué)改變，采用逆轉(zhuǎn)錄-聚合酶鏈?zhǔn)椒磻?yīng)(RT-PCR)法及免疫組織化學(xué)染色法檢測各組大鼠氣道CCR6mRNA及其蛋白的表達。 結(jié)果①哮喘組、哮喘+煙霧暴露組BALF中白細胞總數(shù)、嗜酸粒細胞、中性粒細胞均高于對照組和煙霧暴露組，，P均0.05；哮喘+煙霧暴露組BALF中白細胞總數(shù)和中性粒細胞高于哮喘組，嗜酸粒細胞低于哮喘組，P均0.05。②哮喘組、哮喘+煙霧暴露組CCR6mRNA及其蛋白表達水平均明顯高于對照組和煙霧暴露組，P均0.01；哮喘+煙霧暴露組CCR6mRNA及其蛋白表達水平明顯高于哮喘組，P均0.01。 結(jié)論氣道粘膜CCR6mRNA及其蛋白高表達提示CCR6可能參與了哮喘大鼠氣道炎癥反應(yīng)；煙霧暴露可通過促使氣道CCR6mRNA及其蛋白表達水平升高，誘發(fā)和加重哮喘大鼠氣道慢性炎癥。
[Abstract]:Objective to study the effect of tobacco smoke exposure on the expression of CCR6 (Chemokinereceptor6) in airway of asthmatic rats, and to explore the immunological mechanism of airway inflammation induced and aggravated by smoking. Methods 40 male Wistar rats were randomly divided into control group, smoke exposure group, asthma group and asthma smoke exposure group with 10 rats in each group. The rat model of asthma and the model of tobacco smoke exposure in asthmatic rats were established. The white blood cell count and cell classification of bronchoalveolar lavage fluid (BALF) were collected and the pathological changes of lung tissue were observed by hematoxylin and eosin (HE) staining. Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical staining were used to detect the expression of CCR6mRNA and its protein in rat airway. Results 1 the total number of leukocytes, eosinophils, neutrophils in BALF in asthma group was higher than that in control group and smoke exposure group (P 0.05), and the total number of leukocyte and neutrophil in asthma smoke exposure group was higher than that in asthma group. Eosinophils were lower than asthma group (P 0.05.2), and the expression of CCR6mRNA and its protein in asthma smoke exposure group were significantly higher than those in control group and smoke exposure group (P 0.01). The expression of CCR6mRNA and its protein in asthmatic smoke exposure group was significantly higher than that in asthma group (P < 0.01). Conclusion the high expression of CCR6mRNA and its protein in airway mucosa suggests that CCR6 may be involved in airway inflammation in asthmatic rats, and smoke exposure may induce and aggravate chronic airway inflammation in asthmatic rats by increasing the expression of CCR6mRNA and its protein in the airway.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2013
【分類號】：R562.25

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本文編號：2141249