阿托伐他汀对哮喘大鼠气道炎症及气道重构的影响

摘要

Objective To observe the effects of atorvastatin on airway inflammation and airway remodeling in rats with asthma caused by ovalbumin.Methods Twenty-four male SD rats were randomly divided into three groups:control group, asthma model group and atorvastatin group,with 8 rats in each group.The rats in control group were given 0.9%sodium chloride solution, the rats in asthma model group were sensitized and stimulated by ovalbumin, however,the rats in atorvastatin group were given orally atorvastatin before sensitization.The airway expiratory resistance was detected by pulmonary function test for the three groups,and the inner circumference and area of bronchus wall,the area of tracheal smooth muscle were measured by image analysis software.The airway collagen deposition was detected by Masson stainingand,and the serum levels of interleukin-13 (IL-13) and transforming growth factorβ1 (TGF-β1) were measured by ELISA.Results The average expiratory resistance in asthma model group was significantly higher than that in control group and atorvastatin group (P <0.05).The pathological examination showed that the airway inflammation in asthma model group was more obvious than that in control group and atorvastatin group.There were significant differences in the area of bronchus wall and the area of tracheal smooth muscle between atorvastatin group and asthma model group ( P <0.05).The collagen deposition in pulmonary tissues in atorvastatin group was significantly decreased,as compared with that in asthma model group ( P <0.05).The expression levels of IL-13 and TGF-β1in atorvastatin group were significantly decreased,as compared with those in asthma model group ( P <0.05).Conclusion Atorvastatin can obviously relieve the airway inflammation and decrease airway basic resistance in rats with asthma,moreover,which can lessen the collagen deposition in lung tissues and decrease the area of bronchus wall and area of tracheal smooth muscle to alleviate airway remodeling.Moreover atorvastatin can decrease the expression levels of IL-13 and TGF-β1, which may be the action mechanism in alleviating inflammation and airway remodeling.%目的：探讨阿托伐他汀对卵清白蛋白致敏哮喘模型大鼠气道炎症和重构的影响。方法清洁级 SD 雄性大鼠24只按随机数字表法分为对照组、哮喘组和阿托伐他汀组，每组8只。对照组大鼠采用0．9％氯化钠溶液（生理盐水）进行致敏和激发，哮喘组大鼠采用卵清白蛋白致敏和激发，阿托伐他汀组在致敏和激发前以阿托伐他汀口服。采用肺功能检测3组大鼠气道呼气阻力；采用图像分析软件测定肺组织切片中的支气管壁内周长、支气管管壁面积、支气管平滑肌面积；胶原表达通过气道壁 Masson 染色进行观察；实验动物血清中白介素－13（IL－13）及转化生长因子－β1（TGF－β1）的水平以 ELISA 法测定。结果肺功能检测显示哮喘组平均呼气阻力显著升高，阿托伐他汀组低于哮喘模型组（ P ＜0．05）；病理检查显示哮喘组气道炎症明显，对照组和阿托伐他汀组与之相比炎症轻微；阿托伐他汀组大鼠气道管壁面积、平滑肌面积图像分析和哮喘组比较差异有统计学意义（ P ＜0．05）；阿托伐他汀组肺组织中胶原沉积表达较哮喘组减少（ P ＜0．05）；阿托伐他汀组大鼠血清中 IL－13和 TGF－β1较哮喘组降低（ P ＜0．05）。结论阿托伐他汀能够明显减轻哮喘大鼠气道炎症，降低哮喘大鼠的气道基本阻力；减少肺组织中胶原沉积，降低气道管壁面积、平滑肌层面积，减轻哮喘气道重构。阿托伐他汀治疗能够降低血清中 TGF －β1和 IL－13水平，或为其减轻炎症和气道重构的机制。