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目的探讨凋亡相关点样蛋白(apoptotic speck-like protein containing a caspase recruitment domain,ASC)在支气管哮喘小鼠肺组织中的表达情况,以及脂多糖(lipopolysaccharide,LPS)对其的调节作用。方法 SPF级雌性C57BL/6小鼠24只,6~8周,18~20 g/只,随机分为3组,分别为PBS对照组(A)、哮喘组(B)、LPS干预组(C)。B、C组小鼠以卵蛋白(OVA)致敏并激发,其中C组在激发前给予10μg/只的LPS腹腔注射,连续3 d;A组用PBS溶液替代OVA致敏和激发。末次激发24 h后,记录各组小鼠的气道反应性监测指标增强呼气间歇(Penh)值。取右上肺组织常规HE染色,光学显微镜下观察组织形态,气管和血管周围炎症细胞浸润情况;行ASC免疫组化,观察其在各组肺组织中的分布情况。采用方差分析进行多组间比较。结果对比A、B组小鼠行为学变化、气道反应性及肺组织病理,显示哮喘小鼠造模成功;C组气道反应性[(1.75±0.46)至(6.53±0.81)]较B组[(4.05±0.22)至(12.07±0.91)]下降,差异有统计学意义(P<0.05);免疫组化提示ASC在哮喘模型中较对照组高表达,而10μg的LPS可明显增加哮喘小鼠中气道上皮的ASC表达。结论 ASC参与哮喘中炎症反应的发生;一定剂量的LPS可加重哮喘小鼠气道上皮炎症,增强ASC在炎症中的参与,但降低哮喘小鼠气道高反应性。
Objective To investigate the expression of apoptotic speck-like protein containing a caspase-encoding domain (ASC) in the lung tissue of asthmatic mice and the regulatory effect of lipopolysaccharide (LPS) on it. Methods Twenty-four female C57BL / 6 mice were randomly divided into three groups: PBS control group (A), asthma group (B), LPS intervention group (C) ). Groups B and C were sensitized and challenged with ovalbumin (OVA). Group C received intraperitoneal injection of LPS 10μg / L for 3 days before challenge. Group A was treated with PBS instead of OVA sensitization and challenge. After 24 h of the last challenge, airway responsiveness monitoring indicators of each group of mice were recorded to enhance the expiratory interval (Penh) value. The normal right upper lung tissue was stained with HE, the morphology of the trachea and the infiltration of inflammatory cells in the perivascular and perivascular tissues were observed under a light microscope. The expression of ASC in the lung tissue was observed by immunohistochemistry. ANOVA was used to compare among groups. Results Compared with group A and group B, the behavior changes, airway reactivity and lung pathology showed that the asthmatic mice were successfully established. The airway responsiveness in group C [(1.75 ± 0.46) vs (6.53 ± 0.81)] was significantly higher than that in group B (4.05 ± 0.22) vs (12.07 ± 0.91)], the difference was statistically significant (P <0.05). Immunohistochemistry showed that ASC was highly expressed in the asthma model compared with the control group, while 10μg LPS significantly increased asthma ASC expression of airway epithelium in mice. Conclusion ASC participates in the inflammatory reaction in asthma. A certain dose of LPS can aggravate airway epithelial inflammation in asthmatic mice and enhance the involvement of ASC in inflammation, but decrease the airway hyperresponsiveness in asthmatic mice.