本文關(guān)鍵詞： 煙草煙霧暴露 N-乙酰半胱氨酸 白介素-17A 白介素-22　出處：《安徽醫(yī)科大學》2016年碩士論文　論文類型：學位論文

【摘要】：目的探討煙草煙霧暴露誘導的肺氣腫小鼠肺組織中白介素-17A(IL-17A)以及白介素-22(IL-22)的變化以及戒煙、N-乙酰半胱氨酸(NAC)對IL-17A和IL-22的影響。方法將雄性BABL/c小鼠,按隨機數(shù)字表法分為正常對照組、煙草煙霧暴露組、戒煙4周組、戒煙8周組、戒煙12周組、NAC灌胃4周組、NAC灌胃8周組,NAC灌胃12周組,每組6只。除正常對照組小鼠以外,其他各組小鼠予以煙草煙霧暴露20周方法。煙草煙霧暴露20周后,隨機抽取正常對照組、煙草煙霧暴露組、戒煙4周組、NAC灌胃4周組、NAC灌胃8周組各1只小鼠進行肺組織切片,低HE染色觀察鏡下解剖結(jié)構(gòu)變化。明確模型組小鼠肺組織發(fā)生肺氣腫病理變化后,處死正常對照組和煙草煙霧暴露組小鼠。對戒煙組小鼠予以停止煙霧吸入。NAC組小鼠予以NAC灌胃處理。于干預4周、8周、12周分別處死相應干預時段戒煙及NAC組小鼠。收集小鼠支氣管肺泡灌洗液(BALF),勻磨肺組織成漿及固定包埋肺組織備用。HE染色觀察肺組織病理學變化。顯微鏡下計數(shù)BALF中白細胞數(shù)目。采用ELISA法檢測肺勻漿及BALF中IL-17A和IL-22濃度。采用SPSS 16.0軟件進行統(tǒng)計學分析,GraphPad Prism 5.0軟件作圖。結(jié)果煙草煙霧暴露20周可使小鼠肺組織發(fā)生肺氣腫樣病理變化,戒煙及NAC灌胃后,肺氣腫變化無明顯改善。煙草煙霧暴露20周組BALF中白細胞數(shù)明顯增多,戒煙4周組BALF中白細胞數(shù)與煙草煙霧暴露組無統(tǒng)計學差異。戒煙8周、12周組及NAC灌胃各組,BALF中白細胞數(shù)較煙草煙霧暴露組明顯下降,仍高于正常對照組水平。與正常對照組相比,煙草煙霧暴露組小鼠肺勻漿及BALF中,IL-17A水平升高(P0.05)。戒煙4周后,肺勻漿及BALF中IL-17A水平均無明顯變化；戒煙8周,肺勻漿及BALF中IL-17A顯著下降,差異有統(tǒng)計學意義；戒煙12周,肺勻漿及BALF中IL-17A水平均下降至正常對照水平。較煙草煙霧暴露組比較,肺勻漿及BALF中,NAC灌胃各組IL-17A水平均明顯下降。較之戒煙4周組,NAC灌胃4周后,肺勻漿及BALF中IL-17A顯著下降。與正常對照組比較,煙草煙霧暴露組肺勻漿及BALF中IL-22水平均明顯升高,戒煙4周后二者中IL-22水平無明顯變化。戒煙8周后,BALF中IL-22水平明顯下降；戒煙12周組,肺勻漿中IL-22顯著下降至正常對照水平。較煙草煙霧暴露組比較,NAC灌胃各組肺勻漿中IL-22水平均下降,且恢復至正常對照水平,差異有統(tǒng)計學意義；BALF中,NAC灌胃各組IL-22水平均較煙草煙霧暴露組下降；且NAC灌胃12周后,IL-22水平恢復至正常對照水平。與戒煙4周組比較,NAC灌胃4周后,小鼠肺勻漿及BALF中工L-22水平均明顯下降。肺勻漿及BALF中IL-22與IL-17A的比值逐漸降低。結(jié)論IL-17A及IL-22與煙草煙霧暴露誘導的小鼠肺組織中慢性炎癥有關(guān)。戒煙及NAC灌胃對煙草煙霧暴露導致的IL-17A及IL-22變化有一定干預作用。
[Abstract]:Objective to investigate the changes of interleukin-17 (IL-17A) and interleukin-22 (IL-22) in lung tissue of emphysema mice induced by tobacco smoke exposure and the effect of N-acetylcysteine on IL-17A and IL-22 in male BABL/c mice. The rats were randomly divided into normal control group, tobacco smoke exposure group, smoking cessation 4 weeks group, smoking cessation 8 weeks group, 12 week smoking cessation group with NAC intragastric perfusion for 12 weeks, each group with 6 rats in each group. Other groups of mice were exposed to tobacco smoke for 20 weeks. After 20 weeks of tobacco smoke exposure, lung tissue sections were randomly selected from normal control group, tobacco smoke exposure group and 4-week smoking cessation group. The changes of anatomical structure under microscope were observed by low HE staining. Mice in the control group and the tobacco smoke exposure group were killed. The mice in the smoking cessation group were given NAC intragastric administration to stop smoke inhalation. The mice in the NAC group and the smoking cessation group were killed at 4 weeks, 8 weeks and 12 weeks, respectively. To collect the bronchoalveolar lavage fluid (BALFN) of mice and to observe the pathological changes of lung tissue by evenly grinding lung tissue pulp and fixed embedding lung tissue. The number of white blood cells in BALF was counted under microscope. The lung homogenate and BALF were detected by ELISA method. The concentrations of IL-17A and IL-22 in mice were analyzed by SPSS 16.0 software. Results the emphysematous pathological changes in lung tissue of mice were induced by tobacco smoke exposure for 20 weeks. After smoking cessation and NAC administration, the changes of emphysema were not significantly improved, and the number of leukocytes in BALF was significantly increased in the group exposed to tobacco smoke for 20 weeks. There was no significant difference in the number of white blood cells in BALF between the smoking cessation group and the tobacco smoke exposure group, but the white blood cell count in the BALF group was significantly lower than that in the tobacco smoke exposure group. The level of IL-17A in lung homogenate and BALF of mice exposed to tobacco smoke was higher than that of normal control group (P 0.05). After 4 weeks of smoking cessation, the level of IL-17A in lung homogenate and BALF did not change significantly, and the level of IL-17A in lung homogenate and BALF did not change after 8 weeks of smoking cessation. The level of IL-17A in lung homogenate and BALF decreased to the normal control level after 12 weeks of smoking cessation, which was significantly lower than that in tobacco smoke exposure group. The levels of IL-17A in lung homogenate and BALF in lung homogenate and BALF group were significantly lower than those in control group. Compared with those in control group, the levels of IL-22 in lung homogenate and BALF in tobacco smoke exposure group were significantly higher than those in control group. There was no significant change in the level of IL-22 in both groups after 4 weeks of smoking cessation, but the level of IL-22 in BALF decreased significantly after 8 weeks of smoking cessation, while in the group of 12 weeks of quitting smoking, the level of IL-22 decreased significantly. The level of IL-22 in lung homogenate was significantly decreased to normal control level, and the level of IL-22 in lung homogenate was lower than that in tobacco smoke exposure group, and returned to normal control level. The levels of IL-22 in each group were significantly lower than those in the group exposed to tobacco smoke, and the level of IL-22 returned to normal level after 12 weeks of NAC administration. The ratio of IL-22 to IL-17A in lung homogenate and BALF decreased gradually. Conclusion IL-17A and IL-22 are related to chronic inflammation in lung tissue induced by tobacco smoke exposure. The changes of IL-17A and IL-22 induced by tobacco smoke exposure have some intervention effect.
【學位授予單位】：安徽醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2016
【分類號】：R563

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