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作 者:黄霂晗 韩佳 徐昌君[1] 欧江琴[1] 林昶[1] 刘杨[1] 丁倩[1] 杨长福[1] HUANG Muhan;HAN Jia;XU Changjun;0U Jiangqin;LIN Chang;LIU Yang;DING Qian;YANG Changfu(Guiyang College of Traditional Chinese Medicine,Guiyang 550002,Guizhou,China)
机构地区:[1]贵阳中医学院
出 处:《辽宁中医药大学学报》2019年第1期47-50,共4页Journal of Liaoning University of Traditional Chinese Medicine
基 金:国家自然科学基金资助项目(81660735)
摘 要:目的:观察黄芪甲苷对肺纤维小鼠肺组织α-平滑肌动蛋白(α-SMA)、Ⅰ型和Ⅲ型胶原表达的影响,并初步探讨黄芪甲苷对小鼠肺纤维化抑制作用的机制。方法:通过于气管内滴注博来霉素(10mL/kg)建立肺纤维化模型,空白组为正常饲养的小鼠,假手术组用生理盐水代替。造模后的C57bl/6小鼠随机分成空白组(正常饲养)、模型组(博来霉素造模+0.5%羧甲基纤维素钠溶液灌胃)、假手术组(生理盐水造模+0.5%羧甲基纤维素钠溶液灌胃)、黄芪甲苷组(博来霉素造模+黄芪甲苷灌胃)和阳性对照地塞米松组(博来霉素造模+地塞米松灌胃),分别于第14天和第28天处死小鼠后取肺组织,行HE染色和Masson染色,观察小鼠肺组织肺纤维化程度,碱性水解法检测小鼠肺组织内羟脯氨酸的含量,免疫组织化学染色法检测小鼠肺组织α-SMA的表达,免疫蛋白印记法检测小鼠肺组织α-SMA、COL1、COL3的表达。结果:与空白组、假手术组相比,模型组肺纤维化分级较高,肺组织炎症反应明显,羟脯氨酸含量明显升高(P<0.05)。与模型组相比,黄芪甲苷组内的羟脯氨酸含量降低(P<0.05),肺组织内α-SMA、COL1、COL3的表达减少(P<0.05),地塞米松组的表达降低不明显(P>0.05)。结论:黄芪甲苷对肺纤维化的干预作用明显,其机制可能与减少成纤维细胞的生成和抑制胶原蛋白的沉积有关。Objective:To investigate the influence of astragaloside Ⅳ on the expression of α-SMA,COL1,COL3 at the pulmonary fibrosis mice and clarify the mechanism underlying the preventive effect of astragaloside Ⅳ on fibrosis in lungs. Methods:C57 bl/6 mice were given the instillation of bleomycin(10 mL/kg)to make a pattern of pulmonary fibrosis,while the control group were the untreated mice,the sham operation group were given the instillation of NS instead. The mice were divided into five groups randomly:control group(untreated),model group(intratracheal instillation of BLM,plus i.g. of 5% sodium carboxymethyl cellulose),sham operation group(intratracheal instillation of NS,plus i.g. of 5% sodium carboxymethyl cellulose),astragaloside Ⅳ group(intratracheal instillation of BLM,plus i.g. of astragaloside Ⅳ),dexamethasone group(intratracheal instillation of BLM,plus i.g. of dexamethasone).The lungs were harvest on 14 d and 28 d for HE-staining and Masson-staining,the content of hydroxyproline(HYP)in serum was analyzed by the hydroxyproline assay,the expression of α-SMA was deceted by immunohistochemical staining and western blotting. Results:Compared to the control group and sham operation group,the fibrosis ranking,the inflammatory reaction of lung tissues,the content of hydroxyproline in the model group were higher(P<0.05). Compared to the model group,the content of hydroxyproline in the astragaloside Ⅳ group were obviously decreased,also the expression of α-SMA,COL1,COL3 were lower in the lung tissues(P<0.05). While the decrease in dexamethasone group were not obvious(P>0.05).Conclusion:These results suggest that astragaloside Ⅳ could prevent the up-regulation of α-SMA,COL1,COL3 expression in fibrotic lungs of mice,which might be one of the mechanisms underlying the preventive effect of astragaloside Ⅳ on pulmonary fibrosis.
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