本文選題：肺復(fù)康合劑 + 肺纖維化　； 參考：《中國老年學(xué)雜志》2015年09期

【摘要】：目的探討肺復(fù)康合劑對(duì)大鼠肺纖維化的抑制作用及相關(guān)機(jī)制。方法 40只SD雄性大鼠隨機(jī)分為對(duì)照組、模型組、造模+肺復(fù)康組、單純肺復(fù)康組。模型組、造模+肺復(fù)康組氣管灌注博萊霉素(5 mg/kg),而對(duì)照組和單純肺復(fù)康組氣管灌注同等劑量無菌生理鹽水,隨后對(duì)照組和模型組生理鹽水灌胃28 d,造模+肺復(fù)康組、單純肺復(fù)康組肺復(fù)康合劑灌胃(12 ml/kg)28 d。給藥28 d后麻醉處死,計(jì)算各組肺系數(shù)、肺干重/體重變化,檢測肺組織羥脯氨酸(HYP)、一氧化氮(NO)、肺動(dòng)脈血漿NO2-/NO3-含量、丙二醛(MDA)水平,以及Western印跡法檢測誘導(dǎo)型NO合酶(i NOS)、結(jié)締組織生長因子(CTGF)、磷酸化細(xì)胞外信號(hào)調(diào)節(jié)激酶(ERK)表達(dá)水平。結(jié)果與對(duì)照組相比,模型組肺系數(shù)、肺干重/體重、HYP、NO、NO2-/NO3-、MDA、i NOS、CTGF、p-ERK表達(dá)均明顯增高(P0.05);與模型組相比,造模+肺復(fù)康組肺系數(shù)、肺干重/體重、HYP、NO、NO2-/NO3-、MDA、i NOS、CTGF、p-ERK表達(dá)水平均明顯降低,肺纖維化指標(biāo)均明顯改善;單純肺復(fù)康組與對(duì)照組相比,上述指標(biāo)沒有明顯變化(P0.05)。結(jié)論肺復(fù)康合劑通過抑制促纖維化因子i NOS、CTGF表達(dá)及ERK信號(hào)通路,減少博萊霉素所致的應(yīng)激損傷、病理變化、膠原合成,發(fā)揮抑制肺纖維化的藥理作用。
[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.
【作者單位】： 濱州醫(yī)學(xué)院醫(yī)藥研究中心;
【基金】：國家自然科學(xué)基金(81273957) 山東省自然科學(xué)基金(ZR2013HM051) 濱州醫(yī)學(xué)院科技重點(diǎn)計(jì)劃(BY2012KJZD10)
【分類號(hào)】：R285.5

【共引文獻(xiàn)】

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5 程s，

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