| 周 丹,金发光,潘 蕾,李立宏,张 媛,董佳佳.胡黄连苷Ⅱ通过抑制NF-κB/MAPK信号通路减轻过敏性哮喘大鼠炎症反应[J].,2024,(10):1818-1824 |
| 胡黄连苷Ⅱ通过抑制NF-κB/MAPK信号通路减轻过敏性哮喘大鼠炎症反应 |
| Picroside II Reduces Inflammation in Allergic Asthma Rats by Inhibiting NF-κB/MAPK Signaling Pathway |
| 投稿时间：2023-10-23 修订日期：2023-11-18 |
| DOI：10.13241/j.cnki.pmb.2024.10.004 |
| 中文关键词: 胡黄连苷Ⅱ 过敏性哮喘 炎症 NF-κB/MAPK信号通路 |
| 英文关键词: Picroside II Allergic asthma Inflammatory NF-κB/MAPK signaling pathway |
| 基金项目:陕西省重点研发计划-重点产业创新链（群）项目（2022ZDLSF01-10） |
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| 中文摘要: |
| 摘要 目的：探究胡黄连苷Ⅱ对过敏性哮喘大鼠炎症反应以及NF-κB/MAPK信号通路的影响。方法：采用卵清白蛋白致敏和雾化吸入激发构建过敏性哮喘大鼠模型。将建模成功的大鼠随机分为模型组、胡黄连苷Ⅱ组和C16-PAF组，另取未建模健康的大鼠作为对照组，每组8只。胡黄连苷Ⅱ组大鼠在造模成功后每日给予灌胃剂量为80 mg/kg的胡黄连苷Ⅱ，激活剂组（C16-PAF组）大鼠每日给予灌胃剂量为80 mg/kg的胡黄连苷Ⅱ和50 μL浓度为4 μmol/L的C16-PAF溶液（MAPK激活剂），共给药14天。模型组大鼠同时给予灌胃等量的生理盐水，对照组大鼠分别在造模和给药同期给予腹腔注射、雾化吸入和灌胃等量的生理盐水。采用全身体积描记法记录大鼠肺功能指标FVC、PEF、FEV0.3以及FEV0.3/FVC。通过苏木精-伊红（HE）染色检测大鼠肺组织病理学变化。采用瑞氏染色分析大鼠肺泡灌洗液（BALF）中白细胞、淋巴细胞、嗜酸性粒细胞和中性粒细胞计数。采用ELISA法检测大鼠血清中OVA-IgE和ET-1水平和BALF中炎性因子IL-4、IL-5、IL-13和IFN-γ水平。采用免疫组织化学染色法分析大鼠肺组织中p-p38MAPK和p-NF-κBp65表达水平。采用Western blot检测大鼠肺组织NF-κB/MAPK信号通路相关蛋白表达水平。结果：对照组大鼠肺组织基本结构和形态均正常，未见炎性细胞浸润和组织病变；模型组大鼠肺组织出现明显的炎性细胞浸润，支气管腔壁显著增厚、管腔缩小，肺泡壁增厚且破坏严重；胡黄连苷Ⅱ组大鼠肺组织炎性细胞浸润、肺泡和支气管结构损伤改善明显；C16-PAF组大鼠肺组织出现与模型组大鼠类似的组织损伤情况，但严重程度稍微降低。与对照组比较，模型组大鼠的FVC、FEV0.3、FEV0.3/FVC和PEF值均降低（P<0.05），BALF中淋巴细胞、嗜酸性粒细胞、中性粒细胞、白细胞计数、IL-4、IL-5和IL-13均升高（P<0.05），BALF中IFN-γ水平降低（P<0.05），血清中IgE和ET-1水平均升高（P<0.05），肺组织中p-NF-κBp65和p-p38MAPK蛋白表达水平均升高（P<0.05）。与模型组比较，胡黄连苷Ⅱ组大鼠的FVC、FEV0.3、FEV0.3/FVC和PEF值均升高（P<0.05），BALF中淋巴细胞、嗜酸性粒细胞、中性粒细胞、白细胞计数、IL-4、IL-5和IL-13均降低（P<0.05），BALF中IFN-γ水平升高（P<0.05），血清中IgE和ET-1水平均降低（P<0.05），肺组织中p-NF-κBp65和p-p38MAPK蛋白表达均降低（P<0.05）；与胡黄连苷Ⅱ组比较，C16-PAF组大鼠的FVC、FEV0.3、FEV0.3/FVC和PEF值均降低（P<0.05），BALF中淋巴细胞、嗜酸性粒细胞、中性粒细胞、白细胞计数、IL-4、IL-5和IL-13均升高（P<0.05），BALF中IFN-γ水平降低（P<0.05），血清中IgE和ET-1水平均升高（P<0.05），肺组织中p-NF-κBp65和p-p38MAPK蛋白表达水平均升高（P<0.05）。与模型组大鼠比较，C16-PAF组大鼠的各项指标差异均无统计学意义（P>0.05）。结论：胡黄连苷Ⅱ可能通过抑制NF-κB/MAPK信号通路减轻过敏性哮喘大鼠炎症反应进程。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect of Picroside II on inflammatory response and NF-κB/MAPK signaling pathway in rats with allergic asthma. Methods: The rat model of allergic asthma was established by ovalbumin sensitization and aerosol inhalation. The rats with successful modeling were randomly divided into model group, Picroside II group and activator group (C16-PAF group), and the healthy rats without modeling were selected as control group, with 8 rats in each group. After the modeling, the rats in the Picroside II group (C16-PAF group) were given Picroside II at an intragastric dose of 80 mg/kg daily, and the rats in the C16-PAF group were given a daily intragastric dose of 80 mg/kg Picroside II and 50 μL of C16-PAF solution (MAPK activator) at a concentration of 4 μmol/L, and the drug was administered for 14 days for each group. The rats in the model group were given the same amount of normal saline by intragastric administration, while the rats in the control group were given the same amount of normal saline by intraperitoneal injection, atomization inhalation and intragastric administration at the same period of modeling and administration, respectively. The rat lung function index of FVC, PEF, FEV0.3 and FEV0.3/FVC were recorded by whole body plethysmography. The pathological changes of rat lung were detected by hematoxylin-eosin (HE) staining. The counts of leukocytes, lymphocytes, eosinophils and neutrophils in the bronchoalveolar lavage fluid (BALF) of rats were analyzed by Reye's staining. The levels of OVA-IgE and ET-1 in serum and the levels of inflammatory factors IL-4, IL-5, IL-13 and IFN-γ in BALF were detected by ELISA. The expression levels of p-p38MAPK and p-NF-κBp65 in rat lung tissue were analyzed by immunohistochemical staining. The expression level of protein in NF-κB/MAPK signaling pathway were detected by Western blot. Results: In the control group, the basic structure and morphology of rat lung tissue were normal, and no inflammatory cell infiltration and tissue lesion were observed. In the model group, there was obvious inflammatory cell infiltration in rat lung tissue, and the wall of bronchial cavity was thickened, the lumen was shrunk, and the wall of alveolar cavity was thickened and severely damaged. The infiltration of lung inflammatory cells and the damage of alveolar and bronchial structures were significantly improved in the Picroside II group. The injury of lung tissue in the C16-PAF group was similar to that in the model group, but the severity was slightly reduced. Compared with control group, the values of FVC, FEV0.3, FEV0.3/FVC and PEF in model group were decreased (P<0.05), and the counts of lymphocytes, eosinophils, neutrophils, white blood cells, IL-4, IL-5 and IL-13 in BALF were increased (P<0.05). The levels of IFN-γ in BALF were decreased(P<0.05), IgE and ET-1 levels in serum were increased(P<0.05), and the expression levels of p-NF-κBp65 and p-p38MAPK protein in rat lung tissue were increased(P<0.05). Compared with model group, the values of FVC, FEV0.3, FEV0.3/FVC and PEF in Picroside II group were increased(P<0.05), and the counts of lymphocytes, eosinophils, neutrophils, white blood cells, IL-4, IL-5 and IL-13 in BALF group were decreased(P<0.05). The level of IFN-γ in BALF was increased (P<0.05), IgE and ET-1 levels in serum were decreased(P<0.05), and the expression levels of p-NF-κBp65 and p-p38MAPK in rat lung tissue were decreased (P<0.05). Compared with Picroside II group, the values of FVC, FEV0.3, FEV0.3/FVC and PEF in C16-PAF group were decreased(P<0.05), and the counts of lymphocytes, eosinophils, neutrophils, white blood cell, IL-4, IL-5 and IL-13 in BALF were increased (P<0.05). The level of IFN-γ in BALF was decreased (P<0.05), IgE and ET-1 levels in serum were increased (P<0.05), and the expression levels of p-NF-κBp65 and p-p38MAPK in rat lung tissue were increased(P<0.05). Compared with the model group, there was no significant difference in all indexes in the C16-PAF group(P>0.05). Conclusion: Picroside II may reduce the inflammatory process of asthmatic rats by inhibiting NF-κB/MAPK signaling pathway. |
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