Research Paper Volume 12, Issue 5 pp 4322—4336

Sirt1 antisense long non-coding RNA attenuates pulmonary fibrosis through sirt1-mediated epithelial-mesenchymal transition

Weibin Qian1, , Xinrui Cai2, , Qiuhai Qian3, ,

  • 1 Department of Lung Disease, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250011, Shandong, P.R. China
  • 2 Department of Traditional Chinese Medicine, Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250062, Shandong, P.R. China
  • 3 Department of Endocrinology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250011, Shandong, P.R. China

Received: December 7, 2019       Accepted: February 5, 2020       Published: March 6, 2020
How to Cite

Copyright © 2020 Qian et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Long noncoding RNAs sirt1 antisense (sirt1 AS) was reported to play crucial roles in the progression of organ fibrosis. However, the roles of sirt1 AS in idiopathic pulmonary fibrosis (IPF) are still unknown. In addition, we have previously demonstrated that astragaloside IV (ASV), a bioactive saponin extract of the Astragalus root, significantly alleviates IPF by inhibiting transforming growth factor β1 (TGF-β1) induced epithelial-mesenchymal transition (EMT). Further investigations into the influence of ASV on lncRNAs expression will be helpful to delineate the complex regulatory networks underlying the biological function of ASV. Here, we found sirt1 AS expression was significantly decreased in BLM-induced pulmonary fibrosis. We further found that sirt1 AS effectively inhibited TGF-β1-meidated EMT in vitro and alleviated the progression of IPF in vivo. Mechanistically, sirt1 AS was validate to enhance the stability of sirt1 and increased sirt1 expression, thereby to inhibit EMT in IPF. Furthermore, we demonstrated that ASV treatment increased sirt1 AS expression and silencing of sirt1 AS impaired anti-fibrosis effects of ASV on IPF. Collectively, sirt1 AS was critical for ASV-mediated inhibition of IPF progression and targeting of sirt1 AS by ASV could be a potential therapeutic approach for IPF.


sirt1 AS: Long noncoding RNAs sirt1 antisense; IPF: idiopathic pulmonary fibrosis; ASV: astragaloside IV; TGF-β1: transforming growth factor β1; EMT: epithelial-mesenchymal transition; BLM: bleomycin.