人参皂苷Rh1对哮喘模型小鼠炎症因子表达的抑制作用

目的:观察和探讨人参皂苷Rh1对哮喘模型小鼠的血清和支气管肺泡冲洗液(bronchoalveolar lavage fluid,BALF)中炎症因子的表达和肺组织形态学变化的影响。方法:雄性BALB/c小鼠40只,分为正常对照组、哮喘模型组、人参皂苷Rh1小剂量(40 mg·kg~(-1)·d~(-1))治疗组和人参皂苷Rh1大剂量(80 mg·kg~(-1)·d~(-1))治疗组,并利用卵清蛋白致敏和雾化吸入激发方法制作哮喘模型;人参皂苷Rh1小剂量治疗组和大剂量治疗组分别在每次激发攻击前30 min灌胃,每天一次,共2周。在末次激发24 h后收集BALF,计数嗜酸性粒细胞(eosinophil,EOS)数目;利用ELISA测定BALF中白细胞介素(IL)-4、IL-5和干扰素γ(IFN-γ)的水平;收集血液并测定血清中Ig G和Ig E的水平;用Western blot检测肺组织中转化生长因子(TGF)-β1蛋白表达的变化;用HE染色观察肺组织的病理学变化。结果:人参皂苷Rh1可抑制小鼠哮喘模型BLAF中EOS数目(P0.01);降低BLAF中IL-4、IL-5和IFN-γ的表达(P0.01);减少血清中Ig E的含量(P0.01);减少肺组织中TGF-β1蛋白表达(P0.01),并改善哮喘小鼠肺组织病理学变化。结论:人参皂苷Rh1对哮喘小鼠具有抑制炎症因子表达、调节免疫反应和改善肺组织病理变化的作用。

Effects of ginsenoside Rh1 on expression of inflammatory factors in mouse asthma model

AIM: To observe the effects of ginsenoside Rh1 on the levels of inflammatory factors in serum and bronchoalveolar lavage fluid (BALF), and the pathological changes of the lung tissues in an experimentally induced mouse asthma model. METHODS: Male BALB/c mice (n=40) were divided into 4 groups:normal control group, asthma mo-del group, and low-dose (40 mg·kg^-1·d^-1) and high-dose (80 mg·kg^-1·d^-1) ginsenoside Rh1 groups. The bronchial asthma mouse model was established by the method of ovalbumin induction and excitation, and during the excitation period, the mice were daily treated with ginsenoside Rh1 for 2 weeks. At 24 h after the final dose of ginsenoside Rh1, the mice were sacrificed. The number of eosinophils (EOS) and the concentrations of interleukin (IL)-4, IL-5 and interferon (IFN)-γ in BALF were determined. The levels of IgG and IgE in serum were measured, and the expression of transforming growth factor (TGF)-β1 and the pathological changes in lung tissues were evaluated. RESULTS: Ginsenoside Rh1 inhibited the increases in the number of EOS and the concentrations of IL-4, IL-5, IFN-γ and IgE, reversed the increased expression of TGF-β1, and improved the pathological changes of the lung tissues in asthmatic mice. CONCLUSION: Ginsenoside Rh1 improves the immuno-inflammatory profile and pathological changes in the experimentally induced mouse asthma model, implying its potential therapeutic effect on asthma.