肺复康合剂对大鼠肺纤维化的抑制作用及相关机制

发布时间：2018-06-28 02:53

本文选题：肺复康合剂 + 肺纤维化　；参考：《中国老年学杂志》2015年09期

【摘要】：目的探讨肺复康合剂对大鼠肺纤维化的抑制作用及相关机制。方法 40只SD雄性大鼠随机分为对照组、模型组、造模+肺复康组、单纯肺复康组。模型组、造模+肺复康组气管灌注博莱霉素(5 mg/kg),而对照组和单纯肺复康组气管灌注同等剂量无菌生理盐水,随后对照组和模型组生理盐水灌胃28 d,造模+肺复康组、单纯肺复康组肺复康合剂灌胃(12 ml/kg)28 d。给药28 d后麻醉处死,计算各组肺系数、肺干重/体重变化,检测肺组织羟脯氨酸(HYP)、一氧化氮(NO)、肺动脉血浆NO2-/NO3-含量、丙二醛(MDA)水平,以及Western印迹法检测诱导型NO合酶(i NOS)、结缔组织生长因子(CTGF)、磷酸化细胞外信号调节激酶(ERK)表达水平。结果与对照组相比,模型组肺系数、肺干重/体重、HYP、NO、NO2-/NO3-、MDA、i NOS、CTGF、p-ERK表达均明显增高(P0.05);与模型组相比,造模+肺复康组肺系数、肺干重/体重、HYP、NO、NO2-/NO3-、MDA、i NOS、CTGF、p-ERK表达水平均明显降低,肺纤维化指标均明显改善;单纯肺复康组与对照组相比,上述指标没有明显变化(P0.05)。结论肺复康合剂通过抑制促纤维化因子i NOS、CTGF表达及ERK信号通路,减少博莱霉素所致的应激损伤、病理变化、胶原合成,发挥抑制肺纤维化的药理作用。
[Abstract]:Objective to investigate the inhibitory effect of Feifukang mixture on pulmonary fibrosis in rats and its related mechanism. Methods Forty Sprague-Dawley male rats were randomly divided into control group, model group and simple group. In the model group, bleomycin (5 mg/kg) was perfused into the trachea of the model group, and the same dose of aseptic saline was infused into the trachea of the control group and the simple group, then the control group and the model group were given intragastric administration of saline for 28 days. Feifukang mixture was perfused (12 ml/kg) for 28 days. The lung coefficient, lung dry weight / body weight of each group were calculated after 28 days of administration. The levels of hydroxyproline (HYP), nitric oxide (no), plasma no 2-/ no 3- and malondialdehyde (MDA) in pulmonary artery were measured. The expression of inducible no synthase (iNOS), connective tissue growth factor (CTGF) and phosphorylated signal regulated kinase (ERK) were detected by Western blot. Results compared with the control group, the lung coefficient, lung dry weight / body weight of the model group and the expression of CTGFP-ERK in the model group were significantly higher than those in the model group (P0.05), and the expression of CTGFP-ERK in the model group was significantly lower than that in the model group, and the expression of CTGFP-ERK in the model group was significantly lower than that in the model group, and the expression of CTGFP-ERK in the model group was significantly lower than that in the model group (P < 0.05), and the expression level of CTGFP-ERK in the model group was significantly lower than that in the model group. Pulmonary fibrosis indexes were significantly improved; compared with the control group, there was no significant change in the above indexes (P0.05). Conclusion Feifukang mixture can inhibit the expression of I NOSN CTGF and ERK signal pathway, reduce the stress injury, pathological changes and collagen synthesis induced by bleomycin, and play a pharmacological role in inhibiting pulmonary fibrosis.
【作者单位】：滨州医学院医药研究中心;
【基金】：国家自然科学基金(81273957) 山东省自然科学基金(ZR2013HM051) 滨州医学院科技重点计划(BY2012KJZD10)
【分类号】：R285.5

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