中国现代医学杂志2018，Vol.28Issue(2)：1-7,7.DOI:10.3969/j.issn.1005-8982.2018.02.001
Ac-SDKP通过调节HDAC6和HSP90抑制矽肺纤维化的机制研究
Effect of Ac-SDKP on expressions of HDAC6 and HSP90 in lungs of rats with silicosis
摘要
Abstract
Objective To investigate the effect of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) on the expressions of histone deacetylase 6 (HDAC6) and heat shock protein 90 (HSP90) in the process of fibroblast differentiation. Methods Rats were instilled with silica through trachea to establish silicotic models. The rats were divided into 4-week control group, 4-week silicosis group, 8-week control group, 8-week silicosis group, Ac-SDKP treatment group and Ac-SDKP pre-treatment group. Myofibroblasts induced by TGF-β1 were pre-treated with TCS HDAC620b, the specific inhibitor of Ac-SDKP and HDAC6. Routine HE staining was used to observe the pathomorphology. The expressions of α-SMA, collagen I, HDAC6 and HSP90 were measured by immunohistochemistry and Western blot. Results The expressions of HDAC6 and HSP90 were increased in the silicotic nodules of the rat lungs; upon the treatment or pre-treatment with Ac-SDKP, the expressions of collagen I, α-SMA, HDAC6 and HSP90 were decreased. TGF-β1 induced the α-SMA expression in rat fibroblasts and up-regulated the expressions of HDAC6 and HSP90; moreover, pre-treatment with Ac-SDKP or TCS HDAC620b inhibited the TGF-β1-induced expressions of these factors. Conclusions Ac-SDKP inhibits myofibroblast differentiation and collagen deposition, which is related with regulation of HDAC6 and HSP90.关键词
Ac-SDKP/肺纤维化/HDAC6/HSP90Key words
N-acetyl-seryl-aspartyl-lysyl-proline/fibrosis/HDAC6/HSP90分类
医药卫生引用本文复制引用
李红垒,徐丁洁,郭地利,耿玉聪,高学敏,李世峰,徐洪,杨方,魏中秋..Ac-SDKP通过调节HDAC6和HSP90抑制矽肺纤维化的机制研究[J].中国现代医学杂志,2018,28(2):1-7,7.基金项目
国家自然科学基金(No:81472953) （No:81472953）
河北省自然科学基金(No:H2016209107) （No:H2016209107）
华北理工大学大学生创新项目(No :X2016315) （No :X2016315）
