Arctigenin Suppressed Epithelial-Mesenchymal Transition Through Wnt3a/β-Catenin Pathway in PQ-Induced Pulmonary Fibrosis
Copyright © 2020 Gao, Zhang, Yang, Wang, Zhang, Ren, Han, Wei, Sun and Nie..
Arctigenin (ATG), a major bioactive substance of Fructus Arctii, counters renal fibrosis; however, whether it protects against paraquat (PQ)-induced lung fibrosis remains unknown. The present study was to determine the effect of ATG on PQ-induced lung fibrosis in a mouse model and the underlying mechanism. Firstly, we found that ATG suppressed PQ-induced pulmonary fibrosis by blocking the epithelial-mesenchymal transition (EMT). ATG reduced the expressions of Vimentin and α-SMA (lung fibrosis markers) induced by PQ and restored the expressions of E-cadherin and Occludin (two epithelial markers) in vivo and in vitro. Besides, the Wnt3a/β-catenin signaling pathway was significantly activated in PQ induced pulmonary fibrosis. Further analysis showed that pretreatment of ATG profoundly abrogated PQ-induced EMT-like phenotypes and behaviors in A549 cells. The Wnt3a/β-catenin signaling pathway was repressed by ATG treatment. The overexpression of Wnt3a could weaken the therapeutic effect of ATG in A549 cells. These findings suggested that ATG could serve as a new therapeutic candidate to inhibit or even reverse EMT-like changes in alveolar type II cells during PQ-induced lung fibrosis, and unraveled that the Wnt3a/β-catenin pathway might be a mechanistic tool for ATG to control pulmonary fibrosis.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2020 |
|---|---|
| Erschienen: |
2020 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:11 |
|---|---|
| Enthalten in: |
Frontiers in pharmacology - 11(2020) vom: 28., Seite 584098 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Gao, Fei [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Arctigenin |
|---|
| Anmerkungen: |
Date Revised 05.01.2021 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
|---|
| doi: |
10.3389/fphar.2020.584098 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM319549488 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM319549488 | ||
| 003 | DE-627 | ||
| 005 | 20231225171705.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231225s2020 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.3389/fphar.2020.584098 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1065.xml |
| 035 | |a (DE-627)NLM319549488 | ||
| 035 | |a (NLM)33390951 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Gao, Fei |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Arctigenin Suppressed Epithelial-Mesenchymal Transition Through Wnt3a/β-Catenin Pathway in PQ-Induced Pulmonary Fibrosis |
| 264 | 1 | |c 2020 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Revised 05.01.2021 | ||
| 500 | |a published: Electronic-eCollection | ||
| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a Copyright © 2020 Gao, Zhang, Yang, Wang, Zhang, Ren, Han, Wei, Sun and Nie. | ||
| 520 | |a Arctigenin (ATG), a major bioactive substance of Fructus Arctii, counters renal fibrosis; however, whether it protects against paraquat (PQ)-induced lung fibrosis remains unknown. The present study was to determine the effect of ATG on PQ-induced lung fibrosis in a mouse model and the underlying mechanism. Firstly, we found that ATG suppressed PQ-induced pulmonary fibrosis by blocking the epithelial-mesenchymal transition (EMT). ATG reduced the expressions of Vimentin and α-SMA (lung fibrosis markers) induced by PQ and restored the expressions of E-cadherin and Occludin (two epithelial markers) in vivo and in vitro. Besides, the Wnt3a/β-catenin signaling pathway was significantly activated in PQ induced pulmonary fibrosis. Further analysis showed that pretreatment of ATG profoundly abrogated PQ-induced EMT-like phenotypes and behaviors in A549 cells. The Wnt3a/β-catenin signaling pathway was repressed by ATG treatment. The overexpression of Wnt3a could weaken the therapeutic effect of ATG in A549 cells. These findings suggested that ATG could serve as a new therapeutic candidate to inhibit or even reverse EMT-like changes in alveolar type II cells during PQ-induced lung fibrosis, and unraveled that the Wnt3a/β-catenin pathway might be a mechanistic tool for ATG to control pulmonary fibrosis | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Wnt3a/β-catenin pathway | |
| 650 | 4 | |a arctigenin | |
| 650 | 4 | |a epithelial-mesenchymal transition | |
| 650 | 4 | |a paraquat | |
| 650 | 4 | |a pulmonary fibrosis | |
| 700 | 1 | |a Zhang, Yun |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Zhizhou |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Mengmeng |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Zhiyi |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Wei |e verfasserin |4 aut | |
| 700 | 1 | |a Ren, Yi |e verfasserin |4 aut | |
| 700 | 1 | |a Han, Xiaoqin |e verfasserin |4 aut | |
| 700 | 1 | |a Wei, Mei |e verfasserin |4 aut | |
| 700 | 1 | |a Sun, Zhaorui |e verfasserin |4 aut | |
| 700 | 1 | |a Nie, Shinan |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Frontiers in pharmacology |d 2010 |g 11(2020) vom: 28., Seite 584098 |w (DE-627)NLM208568891 |x 1663-9812 |7 nnns |
| 773 | 1 | 8 | |g volume:11 |g year:2020 |g day:28 |g pages:584098 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.3389/fphar.2020.584098 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 11 |j 2020 |b 28 |h 584098 | ||