Physalin D attenuates hepatic stellate cell activation and liver fibrosis by blocking TGF-β/Smad and YAP signaling.


Journal

Phytomedicine : international journal of phytotherapy and phytopharmacology
ISSN: 1618-095X
Titre abrégé: Phytomedicine
Pays: Germany
ID NLM: 9438794

Informations de publication

Date de publication:
Nov 2020
Historique:
received: 28 01 2020
revised: 14 06 2020
accepted: 24 07 2020
pubmed: 11 8 2020
medline: 1 12 2020
entrez: 11 8 2020
Statut: ppublish

Résumé

Hepatic fibrosis is considered integral to the progression of chronic liver diseases, as it leads to the development of cirrhosis and hepatocellular carcinoma. The activation of hepatic stellate cells (HSCs) is the dominant event in hepatic fibrogenesis. The transforming growth factor-β1 (TGF-β1) and Yes-associated protein (YAP) pathways play a pivotal role in HSC activation, hepatic fibrosis and cirrhosis progression. Therefore, targeting the TGF-β/Smad and YAP signaling pathways is a promising strategy for antifibrotic therapy. The present study investigated the protective effects of Physalin D (PD), a withanolide isolated from Physalis species (Solanaceae), against liver fibrosis and further elucidated the mechanisms involved in vitro and in vivo. We conducted a series of experiments using carbon tetrachloride (CCl PD decreased TGF-β1-induced COL1A1 promoter activity. PD inhibited TGF-β1-induced expression of Collagen I and α-smooth muscle actin (α-SMA) in human hepatic stellate LX-2 cells. PD significantly ameliorated hepatic injury, including transaminase activities, histology, collagen deposition and α-SMA, in CCl These results clearly show that PD ameliorated experimental liver fibrosis by inhibiting the TGF-β/Smad and YAP signaling pathways, indicating that PD has the potential to effectively treat liver fibrosis.

Sections du résumé

BACKGROUND BACKGROUND
Hepatic fibrosis is considered integral to the progression of chronic liver diseases, as it leads to the development of cirrhosis and hepatocellular carcinoma. The activation of hepatic stellate cells (HSCs) is the dominant event in hepatic fibrogenesis. The transforming growth factor-β1 (TGF-β1) and Yes-associated protein (YAP) pathways play a pivotal role in HSC activation, hepatic fibrosis and cirrhosis progression. Therefore, targeting the TGF-β/Smad and YAP signaling pathways is a promising strategy for antifibrotic therapy.
PURPOSE OBJECTIVE
The present study investigated the protective effects of Physalin D (PD), a withanolide isolated from Physalis species (Solanaceae), against liver fibrosis and further elucidated the mechanisms involved in vitro and in vivo.
STUDY DESIGN/METHODS METHODS
We conducted a series of experiments using carbon tetrachloride (CCl
RESULT RESULTS
PD decreased TGF-β1-induced COL1A1 promoter activity. PD inhibited TGF-β1-induced expression of Collagen I and α-smooth muscle actin (α-SMA) in human hepatic stellate LX-2 cells. PD significantly ameliorated hepatic injury, including transaminase activities, histology, collagen deposition and α-SMA, in CCl
CONCLUSION CONCLUSIONS
These results clearly show that PD ameliorated experimental liver fibrosis by inhibiting the TGF-β/Smad and YAP signaling pathways, indicating that PD has the potential to effectively treat liver fibrosis.

Identifiants

pubmed: 32771890
pii: S0944-7113(20)30126-4
doi: 10.1016/j.phymed.2020.153294
pii:
doi:

Substances chimiques

ACTA2 protein, human 0
Actins 0
Adaptor Proteins, Signal Transducing 0
Collagen Type I 0
Collagen Type I, alpha 1 Chain 0
Secosteroids 0
Smad Proteins 0
TGFB1 protein, human 0
Transcription Factors 0
Transforming Growth Factor beta 0
Transforming Growth Factor beta1 0
YAP-Signaling Proteins 0
YAP1 protein, human 0
physalin D 0
Carbon Tetrachloride CL2T97X0V0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

153294

Informations de copyright

Copyright © 2020 Elsevier GmbH. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest No potential conflicts of interest were disclosed.

Auteurs

Dejuan Xiang (D)

State Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China.

Jie Zou (J)

State Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China.

Xiaoyun Zhu (X)

State Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China.

Xinling Chen (X)

State Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China.

Jianguang Luo (J)

State Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China.

Lingyi Kong (L)

State Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China. Electronic address: cpu_lykong@126.com.

Hao Zhang (H)

State Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China. Electronic address: hiaaron@sina.cn.

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Classifications MeSH