摘要: |
[目的] 通过观察紫檀芪(pterostilbene)对博莱霉素诱导肺纤维化大鼠NF-κB/TGF-β1/smad 3信号通路的影响,探讨紫檀芪治疗肺纤维化的作用机制。[方法] 选用健康雄性SD大鼠50只,随机分为空白组、模型组、强的松组、紫檀芪高、低剂量组,每组各10只。采用博莱霉素气管内注射法诱导肺纤维化模型。于给药后第28天留取标本,HE染色进行肺组织病理学观察;酶联免疫法(ELISA法)测定各时期血清中核转录因子-κB(NF-κB)、转化生长因子-β1(TGF-β1)含量;用免疫组化技术检测TGF-β1及smad3的表达。[结果] 与正常组比较,模型组大鼠TGF-β1/smad3含量及NF-κB表达明显升高。与模型组比较,紫檀芪组、泼尼松组大鼠肺组织中NF-κB/TGF-β1/smad 3蛋白表达明显降低。紫檀芪高剂量组大鼠TGF-β1、smad3、NF-κB表达较强的松组减弱。[结论] 紫檀芪能够减轻博莱霉素导致的大鼠肺纤维化程度,其作用机制与调控NF-κB/TGF-β1/smad3信号转导蛋白表达有关。 |
关键词: 紫檀芪 肺纤维化 NF-κB/TGF-β1/smad3 |
DOI:10.11656/j.issn.1673-9043.2019.01.15 |
分类号:R285.5 |
基金项目:国家自然科学基金面上项目(30973705);湖北省自然科学基金资助项目(2009CHB001)。 |
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The impact of pterostilbene on transforming NF-κB/TGF-β1/smad3 signaling pathway of pulmonary fibrosis in rats |
PENG Yanfang1, ZHANG Yingweng1, ZHAO Yingqian2, WANG Xiuping1, AI Wang3
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1.Zhongnan Hospital of Wuhan University, Wuhan 430071, China;2.Hubei University of Traditional Chinese Medicine, Wuhan 430065, China;3.Wuhan University, Wuhan 430071, China
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Abstract: |
[Objective] To study the mechanism of pterostilbene which treatpulmonary fibrosis induced by bleomycin-inducedin rats.[Methods] A single dose of bleomycin was intratracheal injected into the SD rats to induce PF. After injection of bleomycin,the rats were randomly divided into prednisone group,low and highdose Pterostilbene treatment groups and model group. The rats that were instilled with normal saline intratracheally served as the blank group. After the treatment for 28 d,the pulmonary pathologic changes were observed under microscope with hematoxylin-eosin staining. The serum levels of NF-κB,TGF-β1 were determined by enzyme-linked immunosorbent assay (Elisa). The immunohistochemical staining was adopte expressions of TGF-β1 and smad3 in each group.[Results] In Pterostilbene groups of high dose,the expression of TGF-β1,smad3,NF-κB isweakened.[Conclusion] Pterostilbenehas a certain treatmenteffect on the pulmonary fibrosis induced by bleomycin in rats,possibly through controlling NF-κB/TGF-β1/smad3 expression. |
Key words: Pterostilbene pulmonary fibrosis NF-κB/TGF-β1/smad3 |