【摘要】 目的应用丙烯醛建立气道炎症模型,给予依拉普利进行干预,了解其对气道炎症的影响,并探讨核因子(NF-κB)在这一过程中的作用。方法健康雄性SD大鼠24只,随机分为4组,每组6只。A组:空白对照组(吸入生理盐水);B组:依拉普利自身对照组(单纯依拉普利灌胃),依拉普利0.5mg/(kg.d)灌胃;C组:模型组(丙烯醛),大鼠吸入4mg/L丙烯醛,每次3h,每天两次;D组:依拉普利干预组(吸入丙烯醛+依拉普利灌胃),处理同模型组,并给予依拉普利0.5mg/(kg.d)灌胃。21d后处死大鼠,采集标本。采用免疫组化方法检测肺组织中血管紧张素和气道上皮NF-κB p65的表达,并计算NF-κB p65的入核率。采用Western blot方法检测肺组织胞浆中的NF-κB。收集支气管肺泡灌洗液,检测其中的中性粒细胞数,用ELISA的方法检测TNF-α、IL-8。结果免疫组化结果显示模型组大鼠肺组织中AngⅡ、NF-κB p65的表达,NF-κB p65入核率较空白对照组明显增高,依拉普利干预组各项指标较模型组明显减少。Western blot检测发现细胞浆中NF-κB的表达量显著增高(P<0.05),依拉普利干预可以使NF-κB p65的表达有一定程度的降低(P<0.05)。支气管肺泡灌流液(BALF)中中性粒细胞数以及ELISA检测的BALF中的炎性细胞因子IL-8和TNF-α模型组显著高于对照组,依拉普利干预组中均有明显降低(P值均<0.05)。结论在丙烯醛诱导的气道和肺的炎症模型中,AngⅡ起了重要的作用,依拉普利可部分抑制这一炎症反应,其机制可能与它抑制了NF-κB的激活有关。更多还原

【Abstract】 Objective To observe the effect of enalapril on airway inflammation in rat models induced by inhaling acrolein and to explore its mechanism.Methods Twenty-four Sprague-Dawley rats were randomly divided into 4 groups(n=6):① control group(inhaled 0.9% normal saline for 3 hours,twice every day);② enalapril self-control group 〔intragastrically administrated enalapril 0.5 mg/(kg·d)only〕;③ model group(stimulated with 4 mg/L acrolein for 3 hours,twice every day);④ enalapril interventive group 〔inhaled acrolein and intragastrically administrated enalapril 0.5 mg/(kg·d)〕.Lung tissue was acquired after the rats were sacrificed on the 21st day.Histopathology examination of lung tissue section stained with HE.Nuclear factor-κB and angiotensin Ⅱ were assayed by immunohistochemisty.Nuclear factor-κB were also detected by Western blot.IL-8 and TNF-α in BALF were estimated by ELISA.Results Compared with the control group and the enalapril interventive group,the expression of AngⅡ and NF-κB in the model group was significantly increased(all P<0.05).Compared with the control group and the enalapril interventive group,the ratio of NF-κB nuclear translocation in the model group was remarkably increased.Neutrophils and the level of IL-8 and TNF-α in BALF were higher in model group than those in control group.Enalapril can suppress them significantly.Conclusion Acrolein inhalation could upregulate the expression of AngII and NF-κB and also increase nuclear translocation ratio of NF-κB.Enalapril can suppress the airway inflammation induced by acrlein.更多还原