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作 者:齐杰[1] 刘艳超[2] 李清君[1] 陈晓玲[1]
机构地区:[1]河北医科大学病理生理学教研室,河北石家庄050017 [2]河北省胸科医院心脏外科,河北石家庄050041
出 处:《中国中药杂志》2010年第22期3043-3047,共5页China Journal of Chinese Materia Medica
摘 要:目的:观察银杏叶提取物(GbE)对博莱霉素(BLM)所致大鼠肺纤维化的影响,并探讨其作用机制。方法:将SD大鼠随机分对照组、BLM+NS组和BLM+GbE组,每个时间点每组6只。各组分别于给药后14,30 d处死动物。光镜下观察肺组织损伤(HE染色)和肺组织纤维化(M asson染色)的程度;采用生化法测定肺组织中胶原蛋白含量及血浆MDA含量;采用免疫组织化学法和免疫细胞化学法观察肺组织和支气管肺泡灌洗液细胞(BALF)中TGF-β1蛋白表达的变化。结果:与对照组大鼠相比,BLM+NS组大鼠各时间点各指标呈明显变化,提示模型制作成功。与BLM+NS(14 d)组大鼠相比,BLM+GbE(14 d)组大鼠血浆MDA含量,支气管肺泡灌洗液(BALF)细胞TGF-β1蛋白表达显著减少;与BLM+NS(30 d)组大鼠相比,BLM+GbE(30 d)组大鼠肺组织损伤、肺组织纤维化显著减轻,肺胶原含量和血浆MDA含量显著减少,肺组织TGF-1β蛋白表达显著减少,但BALF细胞TGF-β1蛋白表达无明显变化。结论:银杏叶提取物具有抗BLM诱导的大鼠肺纤维化作用,其机制可能与减少纤维化早期(14 d)肺泡巨噬细胞和纤维化期(30 d)肺非炎症细胞TGF-β1蛋白表达及减轻BLM所致的氧化应激有关。Objective: To observe the effect of Ginkgo biloba extract(GbE) against the bleomycin induced pulmonary fibrosis and to investigate its mechanisms.Method: SD rats were randomly divided into 3 groups: Control group,BLM+NS group and BLM+GbE group(n=6 in each time point of each group).Rats in each group were sacrificed on the 14th and 30th day after endotracheal injection of bleomycin A5.Lung injury through HE stain and pulmonary fibrosis through Masson stain were observed by light microscope.The content of collagen protein in lung tissue and malondialdehyde(MDA) in plasma were assayed by biochemical methods.The expressions of TGF-β1 in tissue and bronchoalveolar lavage fluid(BALF) were detected by immunohistochemistry and immunocytochemistry respectively.Result: Compared with control group,every datum in each time point in BLM+NS group showed significant changes which indicated the success of the model.Compared with BLM+NS(14 d) group,MDA in serum and TGF-β1 in alveolar macrophage were significantly reduced in BLM +GbE(14 d) group.The data in BLM +GbE(30 d) group were compared with those in BLM+NS(30 d) group as follows.The lung injury and fibrosis were significantly ameliorated,the content of collagen in lung tissue and MDA in plasma were significantly reduced,the expression of TGF-β1 in lung tissue was significantly reduced,however the expression of TGF-β1 in BALF cells was not significantly changed.Conclusion: GbE inhibited bleomycin induced lung injury and fibrosis in rats.The possible mechanisms were that GbE could inhibit the expression of TGF-β1 in alveolar macrophage in early stage of fibrosis(14 d) and in noninflammatory cells in proliferative stage(30 d),and GbE could also attenuate the oxidative stress induced by bleomycin.
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