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目的通过烟熏法建立大鼠被动吸烟模型,观察香烟烟雾及戒烟对大鼠白介素17(简称IL-17)和肺表面活性物质A(pulmonary surfactant protein A简称SP-A)的变化,探讨IL-17、SP-A在吸烟相关性肺损伤中的作用机制。方法选择健康雄性Wistar大鼠50只,随机分为5组,分别为正常对照组、被动吸烟4周组、被动吸烟8周组、被动吸烟12周组和戒烟组。HE染色观察肺组织的病理改变,免疫组织化学染色方法观察大鼠肺组织中IL-17的表达,采用ELISA方法检测血清中SP-A、IL-17含量。结果香烟烟雾可导致肺组织炎症反应和肺气肿改变;肺组织IL-17表达增强;被动吸烟组和戒烟组大鼠血清SP-A[(4.94±1.90)、(8.80±1.44)、(12.81±3.16)、(10.39±1.92)mg/L和(3.32±0.73)mg/L,F=22.85,P<0.001]、IL-17[(118.29±15.71)、(148.99±17.01)、(175.70±15.40)、(151.31±20.6)pg/L和(98.99±12.26)pg/L,F=33.62,P<0.001]含量较正常对照组升高;随着被动吸烟时间的延长,肺组织中IL-17表达逐渐增加,血清中SP-A、IL-17含量逐渐增加;戒烟组较12周组肺组织中IL-17表达减少,血清SP-A[(10.39±1.92)vs(12.81±3.16),t=-6.42,P<0.05]、IL-17[(151.31±20.6)vs(175.70±15.40),t=-9.43,P<0.05]含量明显降低。结论香烟烟雾可引起肺部炎症,导致肺组织IL-17及血清SP-A、IL-17表达增加。
Objective To establish a rat passive smoking model by smoking method and observe the changes of rat IL-17 and pulmonary surfactant protein A (SP-A) after cigarette smoke and smoking cessation, 17, SP-A in smoking-related lung injury mechanism. Methods Fifty healthy male Wistar rats were randomly divided into five groups: normal control group, passive smoking group for 4 weeks, passive smoking group for 8 weeks, passive smoking group for 12 weeks and smoking cessation group. The pathological changes of lung tissue were observed by HE staining. The expression of IL-17 in lung tissue was observed by immunohistochemical staining. The levels of SP-A and IL-17 in serum were detected by ELISA. Results Cigarette smoke could induce the change of inflammatory reaction and emphysema in lung tissue; the expression of IL-17 in lung tissue was increased; the levels of SP-A in passive smoking group and smoking cessation group were (4.94 ± 1.90), (8.80 ± 1.44), (12.81 (P <0.001), IL-17 [(118.29 ± 15.71), (148.99 ± 17.01), (175.70 ± 3.81) mg / L and (3.32 ± 0.73) mg / 15.40), (151.31 ± 20.6) pg / L and (98.99 ± 12.26) pg / L, respectively, F = 33.62, P <0.001]. Compared with the normal control group, 17 (P <0.05). The levels of SP-A and IL-17 in sera of smoking cessation group were decreased, t = -6.42, P <0.05], IL-17 [(151.31 ± 20.6) vs (175.70 ± 15.40), t = -9.43, P <0.05]. Conclusion Cigarette smoke can cause lung inflammation, leading to increased expression of IL-17 and serum SP-A and IL-17 in lung tissue.