期刊
AGING-US
卷 12, 期 5, 页码 4322-4336出版社
IMPACT JOURNALS LLC
DOI: 10.18632/aging.102882
关键词
idiopathic pulmonary fibrosis; epithelial-mesenchymal transition; antisense lncRNA; sirt1; astragaloside IV
资金
- National Natural Science Foundation of China [81904143, 81704071]
- Taishan Scholars Youth Expert Program of Shandong Province in China [tsqn201812146]
- Key Research and Development Plan of Shandong province [2018GSF119027]
- Young Elite Scientists Sponsorship Program by CAST [CACM-2018-QNRC2-B01, 2019-QNRC2-C01]
- China Postdoctoral Science Foundation [2019T120608, 2019M652462]
- Postdoctoral Innovation Project of Shandong Province [201901014]
- Inheritance Studio of Famous experts in traditional Chinese Medicine in Shandong Province of Qiuhai Qian
- Academic promotion programme of Shandong First Medical University
- Scientific and Technological Development Program of Jinan [201805081, 201805009]
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 beta 1 (TGF-beta 1) 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-beta 1-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.
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