朝药鹿茸提取物对哮喘小鼠p38 MAPK表达及IL-4等的影响

Influence of pilose antler extract of Korean medicine on expression of p38 MAPK pathway and IL-4 of asthmatic mice

目的:探讨朝药鹿茸提取物对支气管哮喘模型小鼠肺组织中p38丝裂原活化蛋白激酶(p38 MAPK)表达的影响。方法:应用卵清蛋白腹腔注射致敏复制小鼠哮喘模型,随机分成正常对照组、哮喘模型组和鹿茸低、中、高剂量组。分别采用酶联免疫吸附法(ELISA)和蛋白质印迹法检测支气管肺泡灌洗液(BALF)中观察炎性细胞以及白细胞介素-4(IL-4)、白细胞介素-5(IL-5)、白细胞介素-13(IL-13)、干扰素-γ(IFN-γ)含量以及肺组织中磷酸化p38 MAPK的变化,并观察肺组织病理学改变。结果:哮喘模型组小鼠BALF中炎性细胞计数、IL-4、IL-5、IL-13水平增高,IFN-γ水平降低;肺组织中磷酸化p38 MAPK表达水平升高,与正常对照组比较差异均有统计学意义(P<0.05)。朝药鹿茸小、中、大剂量组小鼠BALF中炎性细胞计数,IL-4、IL-5、IL-13水平和肺组织中磷酸化p38 MAPK表达水平均明显降低,IFN-γ水平明显上升,与哮喘模型组比较均具有显著差异(P<0.05)。朝药鹿茸提取物能明显减轻哮喘小鼠肺组织病理学改变。结论:朝药鹿茸提取物有效治疗哮喘的作用与抑制哮喘小鼠p38 MAPK信号通路的表达密切有关。

Objective： To study the influence of pilose antler extract of Korean medicine on the expression of p38 MAPK in lung tissues of asthmatic mouse models. Methods： Asthmatic mouse models were established by using intraperitoneal injection of ovalbumin, and then the mice were randomly divided into control group, model group and low, middle and high dose of pilose antler groups. The concentrations of IL-4, IL-5, IL-13 and INF-γ in bronchoalveolar lavage fluid（BALF） were measured by using ELISA, and the changes in phospho-p38 MAPK and pathological alterations in lung tissue were observed too. Results： In model group, the number of inflammatory cells, the concentrations of IL-4, IL-5 and IL-13 in BALF, and the expression of phospho-p38 MAPK were higher than those of control group, while the concentration of IFN-γ in BALF was lower than that of control group（P〈0.05）. The number of inflammatory cells, levels of IL-4, IL-5 and IL-13 level in BALF fluid, and expression of phospho-p38 MAPK of mice in pilose antler groups were decreased, while the IFN-γ level was increased, and the difference between pilose antler groups and model group was significant（P〈0.05）. Pilose antler extract could relieve the pathology changes of lung tissues of mice significantly. Conclusion： The treatment effect of pilose antler extract of Korean medicine on asthma is closely related to the inhibition on expression of p38 MAPK pathway in lung tissues of asthmatic mice.