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      Quantitative proteomics reveals the protective effects of Yinchenzhufu decoction against cholestatic liver fibrosis in mice by inhibiting the PDGFRβ/PI3K/AKT pathway

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          Abstract

          Introduction: Yinchenzhufu decoction (YCZFD) is a traditional Chinese medicine formula with hepatoprotective effects. In this study, the protective effects of YCZFD against cholestatic liver fibrosis (CLF) and its underlying mechanisms were evaluated.

          Methods: A 3, 5-diethoxycarbonyl-1, 4-dihydro-collidine (DDC)-induced cholestatic mouse model was used to investigate the amelioration of YCZFD on CLF. Data-independent acquisition-based mass spectrometry was performed to investigate proteomic changes in the livers of mice in three groups: control, model, and model treated with high-dose YCZFD. The effects of YCZFD on the expression of key proteins were confirmed in mice and cell models.

          Results: YCZFD significantly decreased the levels of serum biochemical, liver injury, and fibrosis indicators of cholestatic mice. The proteomics indicated that 460 differentially expressed proteins (DEPs) were identified among control, model, and model treated with high-dose YCZFD groups. Enrichment analyses of these DEPs revealed that YCZFD influenced multiple pathways, including PI3K-Akt, focal adhesion, ECM–receptor interaction, glutathione metabolism, and steroid biosynthesis pathways. The expression of platelet derived growth factor receptor beta (PDGFRβ), a receptor associated with the PI3K/AKT and focal adhesion pathways, was upregulated in the livers of cholestatic mice but downregulated by YCZFD. The effects of YCZFD on the expression of key proteins in the PDGFRβ/PI3K/AKT pathway were further confirmed in mice and transforming growth factor-β-induced hepatic stellate cells. We uncovered seven plant metabolites (chlorogenic acid, scoparone, isoliquiritigenin, glycyrrhetinic acid, formononetin, atractylenolide I, and benzoylaconitine) of YCZFD that may regulate PDGFRβ expression.

          Conclusion: YCZFD substantially protects against DDC-induced CLF mainly through regulating the PDGFRβ/PI3K/AKT signaling pathway.

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          We describe a method, filter-aided sample preparation (FASP), which combines the advantages of in-gel and in-solution digestion for mass spectrometry-based proteomics. We completely solubilized the proteome in sodium dodecyl sulfate, which we then exchanged by urea on a standard filtration device. Peptides eluted after digestion on the filter were pure, allowing single-run analyses of organelles and an unprecedented depth of proteome coverage.
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            Molecular and cellular mechanisms of liver fibrosis and its regression

            Tatiana Kisseleva, David Brenner (2020)
            Chronic liver injury leads to liver inflammation and fibrosis, through which activated myofibroblasts in the liver secrete extracellular matrix proteins that generate the fibrous scar. The primary source of these myofibroblasts are the resident hepatic stellate cells. Clinical and experimental liver fibrosis regresses when the causative agent is removed, which is associated with the elimination of these activated myofibroblasts and resorption of the fibrous scar. Understanding the mechanisms of liver fibrosis regression could identify new therapeutic targets to treat liver fibrosis. This Review summarizes studies of the molecular mechanisms underlying the reversibility of liver fibrosis, including apoptosis and the inactivation of hepatic stellate cells, the crosstalk between the liver and the systems that orchestrate the recruitment of bone marrow-derived macrophages (and other inflammatory cells) driving fibrosis resolution, and the interactions between various cell types that lead to the intracellular signalling that induces fibrosis or its regression. We also discuss strategies to target hepatic myofibroblasts (for example, via apoptosis or inactivation) and the myeloid cells that degrade the matrix (for example, via their recruitment to fibrotic liver) to facilitate fibrosis resolution and liver regeneration.
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              Involvement of PI3K/Akt pathway in cell cycle progression, apoptosis, and neoplastic transformation: a target for cancer chemotherapy.

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              The PI3K/Akt signal transduction cascade has been investigated extensively for its roles in oncogenic transformation. Initial studies implicated both PI3K and Akt in prevention of apoptosis. However, more recent evidence has also associated this pathway with regulation of cell cycle progression. Uncovering the signaling network spanning from extracellular environment to the nucleus should illuminate biochemical events contributing to malignant transformation. Here, we discuss PI3K/Akt-mediated signal transduction including its mechanisms of activation, signal transducing molecules, and effects on gene expression that contribute to tumorigenesis. Effects of PI3K/Akt signaling on important proteins controlling cellular proliferation are emphasized. These targets include cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors. Furthermore, strategies used to inhibit the PI3K/Akt pathway are presented. The potential for cancer treatment with agents inhibiting this pathway is also addressed.
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                Author and article information

                Contributors
                Qian Meng: URI : https://loop.frontiersin.org/people/1023392/overviewRole: Role: Role: Role: Role:
                Hongwen Zhu: URI : https://loop.frontiersin.org/people/2619357/overviewRole: Role:
                Yuanyuan Li: URI : https://loop.frontiersin.org/people/507976/overviewRole: Role:
                Xiaotian Peng: Role: Role: Role:
                Tianming Wang: URI : https://loop.frontiersin.org/people/507916/overviewRole: Role: Role:
                Hui Huang: Role: Role: Role: Role:
                Hu Zhou: URI : https://loop.frontiersin.org/people/352344/overviewRole: Role: Role: Role: Role:
                Yuejia Liu: Role: Role:
                Sujie Ru: Role: Role:
                Jiasheng Wu: URI : https://loop.frontiersin.org/people/2581371/overviewRole: Role: Role: Role:
                Yueming Ma: URI : https://loop.frontiersin.org/people/379851/overviewRole: Role: Role: Role:
                Journal
                Journal ID (nlm-ta): Front Pharmacol
                Journal ID (iso-abbrev): Front Pharmacol
                Journal ID (publisher-id): Front. Pharmacol.
                Title: Frontiers in Pharmacology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1663-9812
                Publication date (Electronic): 26 February 2024
                Publication date Collection: 2024
                Volume: 15
                Electronic Location Identifier: 1341020
                Affiliations
                [1] 1 Department of Pharmacology , School of Pharmacy , Shanghai University of Traditional Chinese Medicine , Shanghai, China
                [2] 2 Analytical Research Center for Organic and Biological Molecules , State Key Laboratory of Drug Research , Shanghai Institute of Materia Medica , Chinese Academy of Sciences , Shanghai, China
                [3] 3 University of Chinese Academy of Sciences , Beijing, China
                [4] 4 School of Chinese Materia Medica , Nanjing University of Chinese Medicine , Nanjing, Jiangsu, China
                Author notes

                Edited by: Yi Wu, Nanjing Agricultural University, China

                Reviewed by: Haifeng Wang, Shenyang Pharmaceutical University, China

                Kapil Upadhyay, University of Michigan, United States

                Hongxu Du, Southwest University, China

                *Correspondence: Jiasheng Wu, wujiasheng@ 123456shutcm.edu.cn ; Yueming Ma, mayueming_117@ 123456hotmail.com
                Article
                Publisher ID: 1341020
                DOI: 10.3389/fphar.2024.1341020
                PMC ID: 10926276
                PubMed ID: 38469403
                SO-VID: cbf64413-dd16-4551-9e25-e46bd2306bb0
                Copyright © Copyright © 2024 Meng, Zhu, Li, Peng, Wang, Huang, Zhou, Liu, Ru, Wu and Ma.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 19 November 2023
                Date accepted : 25 January 2024
                Funding
                The authors declare financial support was received for the research, authorship, and/or publication of this article. This study is funded by the National Natural Science Foundation of China (No. 81773871) and SIMM-SHUTCM Traditional Chinese Medicine Innovation Joint Research Program (Grant No. E2G804H).
                Categories
                Subject: Pharmacology
                Subject: Original Research
                Custom metadata
                section-at-acceptance Ethnopharmacology

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: yinchenzhufu decoction,proteomics,cholestasis,liver fibrosis,pdgfrβ/pi3k/akt
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: yinchenzhufu decoction, proteomics, cholestasis, liver fibrosis, pdgfrβ/pi3k/akt

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