| 引用本文:彭艳芳，张莹雯，张亚兵，叶太生，王秀萍.紫檀芪对博来霉素诱导的肺纤维化大鼠上皮间质转化的影响[J].世界中医药,2020,(18):. |
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| 紫檀芪对博来霉素诱导的肺纤维化大鼠上皮间质转化的影响 |
| Effects of Pterostilbene on Epithelial-to-mesenchymal Transition in Bleomycin-induced Rats with Pulmonary Fibrosis |
| 投稿时间：2020-07-20 |
| DOI：10.3969/j.issn.1673-7202.2020.18.004 |
| 中文关键词: 紫檀芪 Ⅰ、Ⅲ型胶原 肺纤维化 上皮间质转化 细胞外基质 |
| English Keywords:Pterostilbene Type Ⅰ and Ⅲ collagen Pulmonary fibrosis Epithelial-mesenchymal transition Extracellular matrix |
| 基金项目:湖北省卫生计生委中医药科研基金面上项目（ZY2019M080）；第六批全国老中医药专家学术经验继承工作项目（国中医药人教发[2017]29号） |
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| 中文摘要: |
| 目的：观察紫檀芪（Pterostilbene，PTE）对博来霉素诱导的大鼠肺纤维化进程中上皮间质转化（EMT）的抑制作用及其可能机制。方法：选取40只SD大鼠随机分为4组，分别为正常组、模型组、紫檀芪组及泼尼松组。除正常组外，其余组采用气管内注射博来霉素溶液制备大鼠肺纤维化模型。紫檀芪组给予30 mg/(kg·d)紫檀芪溶液灌胃，泼尼松组给予3 mg/（kg·d）泼尼松溶液灌胃，正常组和模型组予以等量DMSO溶剂灌胃，连续21 d。取肺组织行天狼猩红染色观察大鼠肺组织中Ⅰ型胶原(Collagen Ⅰ)、Ⅲ型胶原(Collagen Ⅲ)的分布情况；免疫组化和PCR检测大鼠肺组织α-平滑肌肌动蛋白（α-SMA）、上皮细胞钙连蛋白(E-cadherin)、波形蛋白（Vimentin）的表达。结果：与正常组比较，模型组Col-Ⅰ、Col-Ⅲ的分布均增多，Vimentin、α-SMA蛋白和mRNA的表达升高，E-cadherin蛋白和mRNA的表达下降。与模型组比较，药物组Ⅰ、Ⅲ型胶原的分布均减少，同时上调E-cadherin的mRNA及蛋白表达水平，抑制α-SMA、Vimentin的mRNA及蛋白表达水平。结论:紫檀芪能有效缓解肺纤维化大鼠的纤维化进程，其机制可能与抑制胶原形成以及调控EMT相关分子的表达有关。 |
| English Summary: |
| To observe the inhibitory effects of Pterostilbene(PTE)on Epithelial-to-mesenchymal transition(EMT)in bleomycin-induced pulmonary fibrosis in rats and its possible mechanism.Methods:A total of 40 SD rats were randomly divided into 4 groups：a normal group，a model group，a PTE group and a prednisone group.Except for the normal group，the rat pulmonary fibrosis model was prepared by intratracheal injection of bleomycin solution.30 mg/(kg·d)of PTE was given to the PTE group，3 mg/(kg·d)of prednisone was given to the prednisone group，and the normal group and the model group were given the same amount of DMSO for 21 days.Take the lung tissue and stain it with Sirius scarlet to observe the distribution of collagen type Ⅰ(Collagen Ⅰ)and collagen type Ⅲ(Collagen Ⅲ)in rat lung tissue.Immunohistochemistry and PCR detected the expression of a-SMA，E-cadherin and Vimentin in rat lung.Results:Compared with normal group，the distribution of Col-Ⅰand Col-Ⅲ in the model group were increasing.Vimentin，a-SMA higher protein and mRNA expression were rising.The expression of E-cadherin protein and mRNA decreased.Compared with the model group，the distribution of type Ⅰ and type Ⅲ collagen in the drug group was reduced，and at the same time the mRNA of E-cadherin and protein expression levels were up-regulated，and the mRNA of α-SMA、Vimentin and protein expression level were inhibited.Conclusion:PTE can effectively alleviate the fibrosis process of pulmonary fibrosis rats.The mechanism may be related to the inhibition of collagen formation and the regulation of the expression of EMT-related molecules. |
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