脂氧素A4受体激动剂BML-111对哮喘小鼠气道重塑的作用研究  

Effect of lipoprotein A4 receptor agonist BML-111 on airway remodeling in asthma mice

作　　者：李鑫[1] 刘圆圆 张才擎 LI Xin;LIU Yuan-yuan;ZHANG Cai-qing(Clinical Medical College,Weifang Medical University,Weifang 261053,Shandong Province,China;Department of Respiratory,The Second Affiliated Hospital of Shandong First Medical University,Taian 271000,Shandong Province,China;Department of Respiratory,Shandong Provincial Qianfoshan Hospital Affiliated to Shandong University,Jinan 250014,Shandong Province,China)

机构地区：[1]潍坊医学院临床医学院,山东潍坊261053 [2]山东第一医科大学第二附属医院呼吸内科,山东泰安271000 [3]山东大学附属千佛山医院呼吸内科,山东济南250014

出　　处：《中国临床药理学杂志》2020年第7期779-781,共3页The Chinese Journal of Clinical Pharmacology

基　　金：山东省自然科学基金资助项目(ZR2014HLL003)。

摘　　要：目的研究脂氧素A4受体激动剂(BML-111)在哮喘小鼠气道重塑的作用及其机制。方法按照体重将小鼠随机分为3组:正常组、模型组和实验组,每组10只。通过卵清蛋白(OVA)致敏激发制备小鼠气道重塑模型。在OVA激发前,实验组小鼠腹腔注射BML-111(1μg·g-1),模型组和正常组腹腔注射0.9%NaCl。苏木精-伊红染色在光学显微镜下观察小鼠肺组织病理学变化,以蛋白质印迹法检测小鼠肺组织中α-平滑肌肌动蛋白(α-SMA)、Ⅰ型胶原(collagenⅠ)蛋白和丝苏氨酸蛋白激酶(Akt)磷酸化水平。结果实验组小鼠的管壁厚度、管腔狭窄和炎症细胞浸润程度较模型组明显减弱。正常组、模型组和实验组的α-SMA相对表达量分别为1.00±0.00,4.42±0.71和3.00±0.45;这3组的collagenⅠ相对表达量分别为1.00±0.00,3.90±0.34和2.04±0.53;这3组的p-Akt相对表达量分别为1.00±0.00,2.12±0.38和1.63±0.23。上述指标:模型组与正常组比较,差异均有统计学意义(均P<0.05);实验组与模型组比较,差异均有统计学意义(均P<0.05)。结论 BML-111能减轻哮喘小鼠气道重塑,可能是通过Akt通路发挥作用。Objective To investigate the effect and mechanism of lipoxin A4 receptor agonist BML-111 on airway remodeling in asthma mice.Methods The mice were randomly divided into three groups according to weight:Normal group, model group and experimental group.The ovalbumin(OVA)was used to establish the asthma model.The mice in experiment group were given intraabdominal injection of BML-111(1 μg·g-1)before OVA challenge.Saline was used to replace OVA in normal and model group.Hematoxylin and eosin(HE)staining was used to observe the change of pathology in mice.The protein expression of alpha-smooth muscle action(α-SMA),typeⅠcollagen(collagenⅠ)and phosphorylated serine threonine protein kinase(Akt)in the lung tissue were evaluated by Western blot.Results Compared with model group, the thickness of the wall,the stenosis of the lumen and the infiltration of inflammatory cells in mice were obviously weakened in experimental group.The relative expression of the α-SMA in the normal group, model group and experimental group were 1.00±0.00,4.42±0.713.00±0.45;the relative expression of the collagen Ⅰ in the three groups were 1.00±0.00,3.90±0.34,2.04±0.53;the relative expression of the p-Akt in the three groups were 1.00±0.00,2.12±0.38,1.63±0.23.Comparing between model group and normal group,the difference of the factors were significant(all P < 0.05);comparing between experimental group and model group,the difference of the factors were significant(all P < 0.05).Conclusion BML-111 can alleviate airway remodeling in asthma model.It works may through Akt pathway.

关 键 词：脂氧素A4受体激动剂(BML-111) 哮喘 气道重塑 丝苏氨酸蛋白激酶 气道炎症 

分 类 号：R97[医药卫生—药品]