朝医补肺元汤对哮喘模型小鼠肺组织中p38蛋白激酶表达的影响
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摘要
目的:探讨朝医补肺元汤对小鼠哮喘模型肺组织中p38蛋白激酶表达的作用及其可能机制。方法:雄性BALB/c小鼠40只随机分成5组。支气管肺泡灌洗液(BALF)中IL-5、IL-13的含量采用酶联免疫吸附法(ELISA)测出,并对支气管肺泡灌洗液中炎症细胞的病理学改变进行观察。应用免疫蛋白质印迹(Western blot)测小鼠肺组织中磷酸化的p38MAPK表达作用强弱。结果:相较于正常对照组,哮喘模型组小鼠BALF中IL-5、IL-13以及肺组织中的磷酸化p38MAPK表达增强(P<0.05)。相比较于小鼠哮喘模型组,朝医补肺元汤低、高剂量组小鼠肺泡灌洗液中的IL-5、IL-13、肺组织磷酸化p38MAPK表达水平显著降低(P<0.05)。综上可证明朝医补肺元汤能显著改善哮喘小鼠肺组织的病理学上的改变。结论:朝医补肺元汤显著治疗哮喘的功效密切相关于阻碍哮喘小鼠p38MAPK信号通路的表达。
Objective: To investigate the effect of traditional Korean medicine Bufeiyuan Decoction on the expression of p38 protein kinase in lung tissue of mice with asthma and its possible mechanism. Methods: Forty BALB/c male mice were randomly divided into 5 groups. The levels of IL-5 and IL-13 in bronchoalveolar lavage fluid(BALF) were measured by enzyme-linked immunosorbent assay(ELISA),and the pathological changes of inflammatory cells in bronchoalveolar lavage fluid were observed.The expression of phosphorylated p38 MAPK in lung tissue was measured by Western blot. Results: Compared with the normal control group,IL-5 and IL-13 in BALF and the expression of phosphorylated p38 MAPK in lung tissue in asthmatic model group were increased(P < 0. 05). Compared with the asthmatic model group,IL-5 and IL-13 in BALF and the expression of phosphorylated p38 MAPK in lung tissue in traditional Korean medicine Bufeiyuan Decoction high and low groups were significantly decreased(P < 0. 05). In summary,it can be proved that the treatment of traditional Korean medicine Bufeiyuan Decoction can significantly improve the pathologic changes of lung tissue in asthmatic mice. Conclusion: The effect of the treatment of asthma is significantly related to the expression of p38 MAPK signaling pathway in asthmatic mice. The treating method of traditional Korean medicine Bufeiyuan Decoction is by blocking the expression of p38 mapk signaling pathway in asthmatic mice.
Objective: To investigate the effect of traditional Korean medicine Bufeiyuan Decoction on the expression of p38 protein kinase in lung tissue of mice with asthma and its possible mechanism. Methods: Forty BALB/c male mice were randomly divided into 5 groups. The levels of IL-5 and IL-13 in bronchoalveolar lavage fluid(BALF) were measured by enzyme-linked immunosorbent assay(ELISA),and the pathological changes of inflammatory cells in bronchoalveolar lavage fluid were observed.The expression of phosphorylated p38 MAPK in lung tissue was measured by Western blot. Results: Compared with the normal control group,IL-5 and IL-13 in BALF and the expression of phosphorylated p38 MAPK in lung tissue in asthmatic model group were increased(P < 0. 05). Compared with the asthmatic model group,IL-5 and IL-13 in BALF and the expression of phosphorylated p38 MAPK in lung tissue in traditional Korean medicine Bufeiyuan Decoction high and low groups were significantly decreased(P < 0. 05). In summary,it can be proved that the treatment of traditional Korean medicine Bufeiyuan Decoction can significantly improve the pathologic changes of lung tissue in asthmatic mice. Conclusion: The effect of the treatment of asthma is significantly related to the expression of p38 MAPK signaling pathway in asthmatic mice. The treating method of traditional Korean medicine Bufeiyuan Decoction is by blocking the expression of p38 mapk signaling pathway in asthmatic mice.
引文
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[6]郑光馥,齐宏迁,郑明昱,等.朝医补肺元汤对哮喘小鼠肺泡灌洗液中白细胞介素-4和γ干扰素水平的影响[J].延边大学医学学报,2012,35(2):83-85.
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[8]Ping Hu,Angel R Nebreda,Yan Liu,et al.p38αprotein negatively regulates T helper type 2 responses by orchestratingmultiple T cell receptor-associated signals[J].J Biol Chem,2012,287(40):33215.
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[11]Kumar S,Boehm J,Lee JC.p38MAP kinases:key signalling molecules as therapeutic targets for inflammatory diseases[J].Nat Rev Drug Discov,2003,2(9):717-726.
[12]Je JH,Lee JY,Jung KJ,et al.NF-kappa B activation mechanism of4-hydroxyhexenal via NIK/IKK and p38 MAPK pathway[J].FEBS Lett,2004,566(1/3):
[2]Abraham WM.Tryptase:potential role in airway inflammation and remodeling[J].Am J Physiol Lung Cell Mol Physiol,2002,282(2):193-196.
[3]陈敏,张涛,李永霞.气道炎症氧化应激反应标记物在哮喘患者中的应用[J].临床肺科杂志,2010,15(2):230-231.
[4]黄翠萍,张珍祥,徐永健.哮喘大鼠肺组织p38蛋白激酶表达的变化及地塞米松对其影响[J].中华微生物学和免疫学杂志,2003,23(5):433.
[5]冯晓纯,延光海,郑明昱.朝医山药补肺元汤对哮喘模型小鼠气道炎症的影响[J].中华中医药杂志,2012,8(8):2064-2066.
[6]郑光馥,齐宏迁,郑明昱,等.朝医补肺元汤对哮喘小鼠肺泡灌洗液中白细胞介素-4和γ干扰素水平的影响[J].延边大学医学学报,2012,35(2):83-85.
[7]李锋,周新.丝裂原活化蛋白激酶与慢性气道疾病[J].中华哮喘杂志,2010,8(4):291-293.
[8]Ping Hu,Angel R Nebreda,Yan Liu,et al.p38αprotein negatively regulates T helper type 2 responses by orchestratingmultiple T cell receptor-associated signals[J].J Biol Chem,2012,287(40):33215.
[9]Carvalho H,Evelson P,Sigaud S,et al.Mitogen-activated protein kinases modulate H(2)O(2)-induced apoptosis in primary rat alveolar epithelial cells[J].J Cell Biochem,2004,92(3):502-513.
[10]Schindler JF,Monahan JB,Smith WG.p38 pathway kinases as antiinflammatory drug targets[J].J Dent Res,2007,86(9):800-811.
[11]Kumar S,Boehm J,Lee JC.p38MAP kinases:key signalling molecules as therapeutic targets for inflammatory diseases[J].Nat Rev Drug Discov,2003,2(9):717-726.
[12]Je JH,Lee JY,Jung KJ,et al.NF-kappa B activation mechanism of4-hydroxyhexenal via NIK/IKK and p38 MAPK pathway[J].FEBS Lett,2004,566(1/3):