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川贝母对哮喘模型小鼠气道炎症及ERK/MAPK信号通路的影响
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| 篇名： | 川贝母对哮喘模型小鼠气道炎症及ERK/MAPK信号通路的影响 |
| TITLE： | |
| 摘要： | 目的：考察川贝母对哮喘模型小鼠气道炎症及细胞外信号调节激酶（ERK）/丝裂原活化蛋白激酶（MAPK）信号通路的影响，探讨其治疗哮喘的可能机制。方法：以卵蛋白致敏小鼠建立哮喘模型。将造模成功的40只小鼠随机分为模型组（灌胃0.5％羧甲基纤维素）、阳性对照组（腹腔注射0.5 mg/kg地塞米松）和川贝母低、高剂量组（灌胃9.0、18.0 mg/kg），每组10只；另选10只正常小鼠作为正常组（灌胃0.5％羧甲基纤维素）。每天给药1次，连续28 d。给药结束后，对小鼠支气管肺泡灌洗液（BALF）中总细胞和分类细胞（中性粒细胞、巨噬细胞、淋巴细胞和嗜酸性粒细胞）进行计数；光镜下观察小鼠支气管平滑肌病理组织形态，并进行炎症评分；酶联免疫吸附法测定肺组织中ERK、磷酸化ERK（p-ERK），p38 MAPK、磷酸化p38 MAPK（p-p38 MAPK）活性；Western blot法测定肺组织中ERK、p-ERK、p38 MAPK、p-p38 MAPK蛋白表达；实时荧光定量聚合酶链式反应法测定肺组织中ERK、 p38 MAPK mRNA表达。结果：与正常组比较，模型组小鼠BALF中总细胞计数、分类细胞计数、炎症评分和肺组织中p-ERK、p-p38 MAPK活性均显著升高（P＜0.01），肺组织中p-ERK、p-p38 MAPK蛋白表达以及ERK、p38 MAPK mRNA表达均显著增强（P＜0.01）；与模型组比较，各给药组小鼠上述指标均显著改善（P＜0.05或P＜0.01）。结论：川贝母可改善哮喘模型小鼠气道炎症，其机制可能与抑制ERK/MAPK信号通路的激活有关。 |
| ABSTRACT： | OBJECTIVE： To investigate the effects of Fritillariae cirrhosae bulbus on airway inflammation and ERK/MAPK signal pathway of asthma model mice， and to explore its possible mechanism of the treatment of asthma. METHODS： The asthma model was induced by egg albumin. A total of 40 model mice were randomly divided into model group （0.5％ carboxymethyl cellulose， intragastric administration）， positive control group （0.5 mg/kg dexamethasone， intraperitoneal injection）， Fritillariae cirrhosae bulbus low-dose and high-dose groups （9.0， 18.0 mg/kg， intragastric administration）， with 10 mice in each group. Other 10 normal mice were included in normal group （0.5％ carboxymethyl cellulose， intragastric administration）. They were given medicine once a day for consecutive 28 d. After medication， the number of total cells and differential cells （neutrophils， macrophages， lymphocytes and eosinophils） in bronchoalveolar lavage fluid （BALF） of mice were counted. The pathological morphology of bronchial smooth muscle in mice was observed under light microscope， and the inflammatory score was scored； the activities of ERK， phosphorylated ERK （p-ERK）， p38 MAPK and phosphorylated p38 MAPK （p-p38 MAPK） were measured by ELISA. The protein expression of ERK， p-ERK， p38 MAPK and p-p38 MAPK in lung tissue were determined by Western blot assay. mRNA expression of ERK and p38 MAPK were determined by real time fluorescent quantitative PCR. RESULTS： Compared with normal group， the number of total cells and differential cells in BALF of mice， inflammation score， the activities of p-ERK and p-p38 MAPK in lung tissues were increased significantly of mice in model group （P＜0.01）； the protein expression of p-ERK and p-p38 MAPK， mRNA expression of ERK and p38 MAPK were increased significantly in lung tissue of mice in model group （P＜0.01）. Compared with model group， above indexes of treatment groups were all improved significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： Fritillariae Cirrhosae Bulbus can improve airway inflammation in asthma model mice， the mechanisms of which may be related to inhibiting the activation of ERK/MAPK signal pathway. |
| 期刊： | 2018年第29卷第3期 |
| 作者： | 张羽飞，徐红纳，黄伟，任公平，李厚忠 |
| AUTHORS： | ZHANG Yufei，XU Hongna，HUANG Wei，REN Gongping，LI Houzhong |
| 关键字： | 川贝母；哮喘；气道炎症；细胞外信号调节激酶/丝裂原活化蛋白激酶信号通路；小鼠 |
| KEYWORDS： | Fritillariae cirrhosae bulbus；Asthma；Airway inflammation；ERK/MAPK signal pathway； Mice |
| 阅读数： | 212 次 |
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