中文摘要：

目的观察过敏性哮喘对apoE-/-小鼠动脉粥样硬化（AS）病变发生及发展不同时期的影响。方法取6周龄的apoE-/-小鼠,以卵清蛋白（OVA）致敏后给予雾化吸入,激发哮喘发作以建立过敏性哮喘模型,激发2周后检测小鼠肺部病理改变判断造模是否成功。造模成功后分别于激发2周、4周、8周及16周时处死小鼠,取主动脉根部进行冰冻切片,油红O染色并计算AS斑块相对面积,CD68荧光染色检测斑块内巨噬细胞含量,天狼星红染色检测斑块内胶原含量。结果与对照组相比,过敏性哮喘apoE-/-小鼠主动脉根部在激发2周时就有明显的斑块形成和巨噬细胞浸润,并且随着激发时间的延长,斑块面积和斑块内巨噬细胞含量始终高于对照组,同时斑块内胶原含量下降。结论过敏性哮喘促进apoE-/-小鼠AS斑块的形成和发展,并导致其稳定性降低。

英文摘要：

Objective To investigate the effect of allergic asthma on the pathogenesis and development of atherosclerosis（AS）in apoE-/-mice.Methods Six-week apoE-/-mice were used in the experiment.Allergic asthma model was established by ovalbumin（OVA）sensitization and challenge.After asthma was induced,the model was assessed by lung histopathology and eosinophils counts of BALF.Mice were challenged for 2,4,8 or 16 weeks.Frozen sections of aortic root were examined for AS lesion：the area of lesion by oil red staining,the collagen content by Sirius red staining and the macrophage infiltration by CD68 immunofluorescence staining,respectively.Results The results showed that the allergic asthma mice models were successfully established.The area of aortic root plaque was significantly increased in asthmatic apoE-/-mice compared with that in the control group.Meanwhile,macrophage infiltration was increased but the collagen content was decreased in plaque of asthmatic apoE-/-mice compared with control group.Conclusion Allergic asthma accelerates the formation and development of AS and decreases the stability of plaques in the apoE-/-mice.