Literature DB >> 25434425

Protein extracts of Crassostrea gigas alleviate CCl₄-induced hepatic fibrosis in rats by reducing the expression of CTGF, TGF-β1 and NF-κB in liver tissues.

Jue Zhou1, Yi Liang2, Jie-Xue Pan3, Fang-Fang Wang3, Xian-Ming Lin2, Rui-Jie Ma2, Fan Qu3, Jian-Qiao Fang2.   

Abstract

Hepatic fibrosis may contribute to liver carcinoma and the mortality of patients with hepatic fibrosis is gradually increasing. However, no definitive treatment has been established for hepatic fibrosis. The hepatic fibrotic process is reversible and can be controlled; therefore, the creation of novel and effective therapeutic methods to prevent or reverse the disease is required. The aim of the present study was to identify whether protein extracts from Pacific oysters (PEPO) could alleviate the hepatic fibrosis induced by CCl4 and to examine the mechanisms involved. A total of sixty rats were randomly divided into the following experimental groups: The normal control group; the hepatic fibrosis model group; the high‑dose; medium‑dose; and low‑dose PEPO groups; and the colchicine group. The results indicated that compared with those of the model group, PEPO treatment significantly decreased the serum levels of alanine aminotransferase, aspartate aminotransferase, γ‑glutamyltransferase, alkaline phosphatase, hyaluronic acid, laminin, collagen type IV and procollagen III in rats with hepatic fibrosis. The hematoxylin and eosin staining demonstrated that PEPO markedly alleviated hepatic fibrosis. The experiments using immunohistochemistry, western blotting and quantitative PCR indicated that protein and mRNA expression levels of connective tissue growth factor (CTGF), transforming growth factor β1 (TGFβ‑1) and nuclear factor κB (NF‑κB) in the liver tissues were significantly reduced by PEPO treatment. Therefore, it was concluded that PEPO successfully alleviated hepatic fibrosis induced by CCl4 and reversed the effects of hepatotoxicity by regulating the serum levels of enzymes and decreasing the expression levels of CTGF, TGF‑β1 and NF‑κB in liver tissues. These findings may provide a novel treatment option for patients with hepatic fibrosis in the future.

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Year:  2014        PMID: 25434425     DOI: 10.3892/mmr.2014.3019

Source DB:  PubMed          Journal:  Mol Med Rep        ISSN: 1791-2997            Impact factor:   2.952


  5 in total

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Journal:  Exp Ther Med       Date:  2017-08-17       Impact factor: 2.447

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Authors:  Guoxing Zheng; Changying Jiang; Yulin Li; Dandan Yang; Youcai Ma; Bing Zhang; Xuan Li; Pei Zhang; Xiaoyu Hu; Xueqiang Zhao; Jie Du; Xin Lin
Journal:  Protein Cell       Date:  2018-07-06       Impact factor: 14.870

3.  Effects of Nervilia fordii Extract on Pulmonary Fibrosis Through TGF-β/Smad Signaling Pathway.

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Journal:  Front Pharmacol       Date:  2021-04-19       Impact factor: 5.810

4.  Transient Receptor Potential Vanilloid-1 (TRPV1) Alleviates Hepatic Fibrosis via TGF-β Signaling.

Authors:  Ke Qian; Xiaohua Lei; Guoxing Liu; Yu Fang; Chengzhi Xie; Xiaolong Wu; Qiang Liu; Gao Liu; Zhenyu Cao; Ju Zhang; Tao Kuang; Likun Yan; Jie Fu; Huihui Du; Zhiqiang Liu; Yuan Chu; Ge Xu; Hirofumi Yamamoto; Masaki Mori; Xin M Liang; Xundi Xu
Journal:  Dis Markers       Date:  2022-07-21       Impact factor: 3.464

5.  Ultrastructural Characteristics of Rat Hepatic Oval Cells and Their Intercellular Contacts in the Model of Biliary Fibrosis: New Insights into Experimental Liver Fibrogenesis.

Authors:  Joanna Maria Lotowska; Maria Elzbieta Sobaniec-Lotowska; Dariusz Marek Lebensztejn; Urszula Daniluk; Piotr Sobaniec; Krzysztof Sendrowski; Jaroslaw Daniluk; Joanna Reszec; Wojciech Debek
Journal:  Gastroenterol Res Pract       Date:  2017-07-09       Impact factor: 2.260

  5 in total

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