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Nagilactone D ameliorates experimental pulmonary fibrosis in vitro and in vivo via modulating TGF-β/Smad signaling pathway
Li,Ao1; Xiao,Xiao1; Feng,Zhe Ling2; Chen,Xiuping2; Liu,Li Juan1; Lin,Li Gen2; Lu,Jin Jian2; Zhang,Le Le2,3
2020-01-15
Source PublicationToxicology and Applied Pharmacology
ISSN0041-008X
Volume389
Abstract

Pulmonary fibrosis is a prototypic chronic progressive lung disease with high morbidity and mortality worldwide. Novel effective therapeutic agents are urgently needed owing to the limited treatment options in clinic. Herein, nagilactone D (NLD), a natural dinorditerpenoid obtained from Podocarpus nagi, was found to suppress transforming growth factor-β1 (TGF-β1)-mediated fibrotic process in vitro and bleomycin (BLM)-induced pulmonary fibrosis in vivo. NLD attenuated TGF-β1-induced expression of fibrotic markers including type I and III collagen, fibronectin, α-SMA, and CTGF in human pulmonary fibroblasts (WI-38 VA-13 and HLF-1 cells). Mechanism study indicated that NLD suppressed TGF-β1-induced up-regulation of TβR I, and Smad2 phosphorylation, nuclear translocation, and transcriptional activation. Moreover, NLD ameliorated BLM-induced histopathological abnormalities in the lungs of experimental fibrotic mice, suppressed synthesis of relative fibrotic markers and fibroblast-to-myofibroblast transition, as well as BLM-induced up-regulation of TβR I expression and Smad signaling in mouse lungs. These data collectively support NLD to be a potential therapeutic agent for pulmonary fibrosis.

KeywordBleomycin Fibrotic Process Nagilactone d Pulmonary Fibrosis Tgf-β1
DOI10.1016/j.taap.2020.114882
URLView the original
Indexed BySCIE
WOS Research AreaPharmacology & Pharmacy ; Toxicology
WOS SubjectPharmacology & Pharmacy ; Toxicology
WOS IDWOS:000514021100001
Scopus ID2-s2.0-85078000254
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Cited Times [WOS]:5   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionUniversity of Macau
Corresponding AuthorLin,Li Gen; Lu,Jin Jian; Zhang,Le Le
Affiliation1.College of Pharmacy and Bioengineering,Chongqing University of Technology,Chongqing,China
2.State Key Laboratory of Quality Research in Chinese Medicine,Institute of Chinese Medical Sciences,University of Macau,Macao,Macao
3.School of Medicine,Chengdu University,Chengdu,China
Corresponding Author AffilicationInstitute of Chinese Medical Sciences
Recommended Citation
GB/T 7714
Li,Ao,Xiao,Xiao,Feng,Zhe Ling,et al. Nagilactone D ameliorates experimental pulmonary fibrosis in vitro and in vivo via modulating TGF-β/Smad signaling pathway[J]. Toxicology and Applied Pharmacology,2020,389.
APA Li,Ao,Xiao,Xiao,Feng,Zhe Ling,Chen,Xiuping,Liu,Li Juan,Lin,Li Gen,Lu,Jin Jian,&Zhang,Le Le.(2020).Nagilactone D ameliorates experimental pulmonary fibrosis in vitro and in vivo via modulating TGF-β/Smad signaling pathway.Toxicology and Applied Pharmacology,389.
MLA Li,Ao,et al."Nagilactone D ameliorates experimental pulmonary fibrosis in vitro and in vivo via modulating TGF-β/Smad signaling pathway".Toxicology and Applied Pharmacology 389(2020).
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