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作 者:栾智华 任晋宏 薛慧清 柴智 雷东霖 成雅楠 LUAN Zhihua;REN JINhong;XUE Huiqing;CHAI Zhi;LEI Donglin;CHENG Yanan(Shanxi University of Chinese Medicine,Jinzhong 030619,Shanxi,China)
出 处:《中华中医药学刊》2020年第6期197-200,I0026-I0028,共7页Chinese Archives of Traditional Chinese Medicine
基 金:山西省卫计委科研项目(201601104);山西省黄芪资源产业化及产业国际化协同创新中心项目(HQXTCXZX2016-027);山西中医药大学博士科研启动金项目(2015BK15)。
摘 要:目的观察黄芪糖蛋白(Huang Qi Glycoprotein,HQGP)对肺纤维化小鼠肺组织病理形态、细胞因子及α-平滑肌肌动蛋白(α-SMA)蛋白表达的影响。方法将80只雌性ICR小鼠随机分为空白组、模型组、地塞米松组、HQGP组,每组20只。空白组鼻腔滴注生理盐水,其余3组鼻腔滴注博来霉素(15 mg/kg)诱导肺纤维化,造模后第1天起,各组小鼠给予相应药物腹腔注射,连续治疗14 d。给药后的第7、28天分两批取材,用HE染色和ELISA测定肺组织TNF-α和IL-1β含量来观察对肺泡炎程度的影响;Masson染色评价对肺纤维化程度的影响;采用免疫组化和Western Blot法分别检测肺组织中α-SMA蛋白表达。结果与模型组比较,第7、28天HQGP组小鼠的肺泡炎、肺纤维化程度明显减轻;第7、28天HQGP组小鼠肺组织中α-SMA蛋白表达显著降低(P<0.01)。结论HQGP对肺纤维化的干预机制可能与抑制肺组织中α-SMA的表达有关。Objective To observe the effect of Huangqi(Astragalus)glycoprotein(HQGP)on the pathological morphology,cytokines andα-smooth muscle actin(α-SMA)protein expression in lung tissue of pulmonary fibrosis mice.Methods Eighty female ICR mice were randomly divided into blank group,model group,dexamethasone group and HQGP group with 20 mice in each group.Normal saline was injected into nasal cavity of the mice in the blank group,bleomycin(15 mg/kg)was injected into nasal cavity of the mice in other three groups to induce pulmonary fibrosis.From the first day after the model was established,mice in each group were given intraperitoneal injection of corresponding drugs for 14 consecutive days.Two batches of samples were taken on the 7 th and 28 th day after administration,and the contents of TNF-αand IL-1βin lung tissue were measured by HE staining and ELISA to observe the effect onalveolitis.Masson staining was used to evaluate the effect onpulmonary fibrosis.Immunohistochemistry and Western Blot were used to detect the expression ofα-SMA protein in lung tissue respectively.Results Compared with the model group,the degrees of alveolitis and pulmonary fibrosis in HQGP group mice on the 7 th and 28 th days were significantly reduced.The expression ofα-SMA protein in lung tissue of mice in HQGP group decreased significantly on 7 th and 28 th day(P<0.01).Conclusion The intervention mechanism of HQGP on pulmonary fibrosis may be related to the inhibition ofα-SMA expression in lung tissue.
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