N-乙酰半胱氨酸对烟草烟雾暴露小鼠肺组织中IL-17A及IL-22的影响

发布时间：2018-02-08 11:29

本文关键词： 烟草烟雾暴露 N-乙酰半胱氨酸白介素-17A 白介素-22　出处：《安徽医科大学》2016年硕士论文　论文类型：学位论文

【摘要】：目的探讨烟草烟雾暴露诱导的肺气肿小鼠肺组织中白介素-17A(IL-17A)以及白介素-22(IL-22)的变化以及戒烟、N-乙酰半胱氨酸(NAC)对IL-17A和IL-22的影响。方法将雄性BABL/c小鼠,按随机数字表法分为正常对照组、烟草烟雾暴露组、戒烟4周组、戒烟8周组、戒烟12周组、NAC灌胃4周组、NAC灌胃8周组,NAC灌胃12周组,每组6只。除正常对照组小鼠以外,其他各组小鼠予以烟草烟雾暴露20周方法。烟草烟雾暴露20周后,随机抽取正常对照组、烟草烟雾暴露组、戒烟4周组、NAC灌胃4周组、NAC灌胃8周组各1只小鼠进行肺组织切片,低HE染色观察镜下解剖结构变化。明确模型组小鼠肺组织发生肺气肿病理变化后,处死正常对照组和烟草烟雾暴露组小鼠。对戒烟组小鼠予以停止烟雾吸入。NAC组小鼠予以NAC灌胃处理。于干预4周、8周、12周分别处死相应干预时段戒烟及NAC组小鼠。收集小鼠支气管肺泡灌洗液(BALF),匀磨肺组织成浆及固定包埋肺组织备用。HE染色观察肺组织病理学变化。显微镜下计数BALF中白细胞数目。采用ELISA法检测肺匀浆及BALF中IL-17A和IL-22浓度。采用SPSS 16.0软件进行统计学分析,GraphPad Prism 5.0软件作图。结果烟草烟雾暴露20周可使小鼠肺组织发生肺气肿样病理变化,戒烟及NAC灌胃后,肺气肿变化无明显改善。烟草烟雾暴露20周组BALF中白细胞数明显增多,戒烟4周组BALF中白细胞数与烟草烟雾暴露组无统计学差异。戒烟8周、12周组及NAC灌胃各组,BALF中白细胞数较烟草烟雾暴露组明显下降,仍高于正常对照组水平。与正常对照组相比,烟草烟雾暴露组小鼠肺匀浆及BALF中,IL-17A水平升高(P0.05)。戒烟4周后,肺匀浆及BALF中IL-17A水平均无明显变化；戒烟8周,肺匀浆及BALF中IL-17A显著下降,差异有统计学意义；戒烟12周,肺匀浆及BALF中IL-17A水平均下降至正常对照水平。较烟草烟雾暴露组比较,肺匀浆及BALF中,NAC灌胃各组IL-17A水平均明显下降。较之戒烟4周组,NAC灌胃4周后,肺匀浆及BALF中IL-17A显著下降。与正常对照组比较,烟草烟雾暴露组肺匀浆及BALF中IL-22水平均明显升高,戒烟4周后二者中IL-22水平无明显变化。戒烟8周后,BALF中IL-22水平明显下降；戒烟12周组,肺匀浆中IL-22显著下降至正常对照水平。较烟草烟雾暴露组比较,NAC灌胃各组肺匀浆中IL-22水平均下降,且恢复至正常对照水平,差异有统计学意义；BALF中,NAC灌胃各组IL-22水平均较烟草烟雾暴露组下降；且NAC灌胃12周后,IL-22水平恢复至正常对照水平。与戒烟4周组比较,NAC灌胃4周后,小鼠肺匀浆及BALF中工L-22水平均明显下降。肺匀浆及BALF中IL-22与IL-17A的比值逐渐降低。结论IL-17A及IL-22与烟草烟雾暴露诱导的小鼠肺组织中慢性炎症有关。戒烟及NAC灌胃对烟草烟雾暴露导致的IL-17A及IL-22变化有一定干预作用。
[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.
【学位授予单位】：安徽医科大学
【学位级别】：硕士
【学位授予年份】：2016
【分类号】：R563

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