五味子乙素通过AKT-mTOR通路减轻博来霉素诱导的小鼠肺纤维化。
Schisandrin B attenuates bleomycin-induced pulmonary fibrosis in mice through AKT-mTOR pathway.
作者信息
Yang Jie, Zhou Dengfeng, Hu Jianwu, Yang David H, Cai Yuanping, Lu Qiaofa
机构信息
Department of Pulmonary and Critical Care Medicine ,Wuhan Fourth Hospital, Wuhan, Hubei Province, China.
Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
出版信息
Sarcoidosis Vasc Diffuse Lung Dis. 2024 Sep 24;41(3):e2024034. doi: 10.36141/svdld.v41i3.12728.
PURPOSE
Schisandrin B (Sch B) is an active monomer of Schisandrin with anti-fibrosis pharmacological action. The study investigated whether Sch B alleviate bleomycin-induced (BLM-Induced) pulmonary fibrosis in mice and attempted to clarify its anti-fibrosis mechanism.
METHODS
Histopathological examination was performed by H&E staining and immunohistochemistry. The inflammatory cytokines and oxidative stress were determined by ELISA. Western blotting and immunofluorescence were used to investigate the possible molecular mechanism to attenuate pulmonary fibrosis by Sch B.
RESULTS
The results indicated that Sch B can significantly attenuate BLM-Induced pulmonary fibrosis, myofibroblast activation, and collagen fibers deposition in mice. In addition, Sch B can inhibit inflammatory response and oxidative stress in early stage. Furthermore, Sch B can inhibit pulmonary fibrosis by promoting autophagy via promoting the dephosphorylation of AKT-mTOR pathway.
CONCLUSIONS
The results suggest that the anti-fibrotic effect of Sch B is potentially related to the activation of autophagy through AKT-mTOR pathway, and Sch B is a potential agent for the treatment of idiopathic pulmonary fibrosis.
目的
五味子乙素（Sch B）是五味子素的一种具有抗纤维化药理作用的活性单体。本研究探讨Sch B是否能减轻博来霉素诱导的小鼠肺纤维化，并试图阐明其抗纤维化机制。
方法
通过苏木精-伊红（H&E）染色和免疫组织化学进行组织病理学检查。采用酶联免疫吸附测定（ELISA）法测定炎性细胞因子和氧化应激。运用蛋白质免疫印迹法和免疫荧光法研究Sch B减轻肺纤维化的可能分子机制。
结果
结果表明，Sch B可显著减轻博来霉素诱导的小鼠肺纤维化、肌成纤维细胞活化和胶原纤维沉积。此外，Sch B可在早期抑制炎症反应和氧化应激。此外，Sch B可通过促进AKT-mTOR通路的去磷酸化来促进自噬，从而抑制肺纤维化。
结论
结果表明，Sch B的抗纤维化作用可能与通过AKT-mTOR通路激活自噬有关，Sch B是治疗特发性肺纤维化的潜在药物。
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