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      Mallotus furetianus extract protects against ethanol‐induced liver injury via the activation of the cAMP‐PKA pathway

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          Abstract

          The protective effects of Mallotus furetianus extract (MF) on liver fibrosis induced with ethanol were examined using in vivo and in vitro model. MF treatment suppressed plasma alanine aminotransferase and aspartate aminotransferase activities in ethanol plus carbon tetrachloride (CCl 4)‐induced cirrhosis rat model. MF also suppressed the increase in type l collagen and α‐smooth muscle actin expression in the livers of ethanol plus CCl4‐induced rat by the maintenance of intracellular glutathione levels. Furthermore, we evaluated the effect of MF on the alcohol‐induced activation of hepatic stellate cells (HSCs), which are responsible for the increased production and deposition of the extracellular matrix in liver injury. Here, we observed the enhancement of the intracellular reactive oxygen species (ROS) levels and the increase in type I collagen and a‐SMA expression in HSCs activated with ethanol. However, the enhanced ROS levels were suppressed with the treatments of MF or diphenyleneiodonium (DPI). Furthermore, the treatment of MF or DPI suppressed the increase in type I collagen and a‐SMA expression activated with ethanol. We also observed that the treatment of MF or LY194002 suppressed the increase in type I collagen expression in HSCs activated with ethanol, suggesting that ethanol induced type I collagen expression via the PI3K‐Akt signaling pathway. On the other hand, the suppression of the synthesis of type I collagen in ethanol and MF‐treated HSCs was inhibited by H‐89. From these results, MF may suppress the increase in the activity of NADPH oxidase in HSCs activated with ethanol through the cAMP‐PKA pathway.

          Abstract

          Mallotus furetianus extract (MF) suppressed the development of alcoholic liver fibrosis. MF suppressed the alcohol‐induced activation of hepatic stellate cells. MF suppressed the increase in the activity of NADPH oxidase in HSCs activated with ethanol through the cAMP‐PKA pathway.

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          Liver fibrosis.

          Ramón Bataller, David A. Brenner (2005)
          Liver fibrosis is the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension and often requires liver transplantation. Our knowledge of the cellular and molecular mechanisms of liver fibrosis has greatly advanced. Activated hepatic stellate cells, portal fibroblasts, and myofibroblasts of bone marrow origin have been identified as major collagen-producing cells in the injured liver. These cells are activated by fibrogenic cytokines such as TGF-beta1, angiotensin II, and leptin. Reversibility of advanced liver fibrosis in patients has been recently documented, which has stimulated researchers to develop antifibrotic drugs. Emerging antifibrotic therapies are aimed at inhibiting the accumulation of fibrogenic cells and/or preventing the deposition of extracellular matrix proteins. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans is unknown. This review summarizes recent progress in the study of the pathogenesis and diagnosis of liver fibrosis and discusses current antifibrotic strategies.
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            Effect of ethanol on lipid metabolism

            Min You, Gavin Arteel (2019)
            Hepatic lipid metabolism is a series of complex processes that control influx and efflux of not only hepatic lipid pools, but also organismal pools. Lipid homeostasis is usually tightly controlled by expression, substrate supply, oxidation and secretion that keep hepatic lipid pools relatively constant. However, perturbations of any of these processes can lead to lipid accumulation in the liver. Although it is thought that these responses are hepatic arms of the ‘thrifty genome’, they are maladaptive in the context of chronic fatty liver diseases. Ethanol is likely unique among toxins, in that it perturbs almost all aspects of hepatic lipid metabolism. This complex response is due in part to the large metabolic demand placed on the organ by alcohol metabolism, but also appears to involve more nuanced changes in expression and substrate supply. The net effect is that steatosis is a rapid response to alcohol abuse. Although transient steatosis is largely an inert pathology, the chronicity of alcohol-related liver disease seems to require steatosis. Better and more specific understanding of the mechanisms by which alcohol causes steatosis may therefore translate into targeted therapies to treat alcohol-related liver disease and/or prevent its progression.
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              Role of NADPH oxidases in the redox biology of liver fibrosis

              Eva Crosas-Molist, Isabel Fabregat (2015)
              Liver fibrosis is the pathological consequence of chronic liver diseases, where an excessive deposition of extracellular matrix (ECM) proteins occurs, concomitantly with the processes of repair and regeneration. It is characterized by increased production of matrix proteins, in particular collagens, and decreased matrix remodelling. The principal source of ECM accumulation is myofibroblasts (MFB). Most fibrogenic MFB are endogenous to the liver, coming from hepatic stellate cells (HSC) and portal fibroblasts. Dysregulated inflammatory responses have been associated with most (if not all) hepatotoxic insults and chronic oxidative stress play a role during the initial liver inflammatory phase and its progression to fibrosis. Redox-regulated processes are responsible for activation of HSC to MFB, as well as maintenance of the MFB function. Increased oxidative stress also induces hepatocyte apoptosis, which contributes to increase the liver injury and to transdifferentiate HSC to MFB, favouring the fibrogenic process. Mitochondria and other redox-active enzymes can generate superoxide and hydrogen peroxide as a by-product in liver cells. Moreover, accumulating evidence indicates that NADPH oxidases (NOXs), which play a critical role in the inflammatory response, may contribute to reactive oxygen species (ROS) production during liver fibrosis, being important players in HSC activation and hepatocyte apoptosis. Based on the knowledge of the pathogenic role of ROS, different strategies to prevent or reverse the oxidative damage have been developed to be used as therapeutic tools in liver fibrosis. This review will update all these concepts, highlighting the relevance of redox biology in chronic fibrogenic liver pathologies.
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                Author and article information

                Contributors
                Akiko Kojima‐Yuasa:
                ORCID: https://orcid.org/0000-0001-8167-3693
                kojima@life.osaka-cu.ac.jp
                Journal
                Journal ID (nlm-ta): Food Sci Nutr
                Journal ID (iso-abbrev): Food Sci Nutr
                Journal ID (doi): 10.1002/(ISSN)2048-7177
                Journal ID (publisher-id): FSN3
                Title: Food Science & Nutrition
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2048-7177
                Publication date (Electronic): 10 June 2020
                Publication date Collection: July 2020
                Volume: 8
                Issue: 7 ( doiID: 10.1002/fsn3.v8.7 )
                Pages: 3936-3946
                Affiliations
                [ 1 ] Department of Food and Human Health Sciences Graduate School of Human Life Science Osaka City University Osaka Japan
                [ 2 ] Department of Pharmacognosy School of Pharmacy Kitasato University Tokyo Japan
                Author notes
                [*] [* ] Correspondence

                Akiko Kojima‐Yuasa, Department of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, Osaka 558‐8585 Japan.

                Email: kojima@ 123456life.osaka-cu.ac.jp

                Author information
                https://orcid.org/0000-0001-8167-3693
                Article
                Publisher ID: FSN31709
                DOI: 10.1002/fsn3.1709
                PMC ID: 7382178
                SO-VID: b00fa293-3718-4c09-a540-44057437cd28
                Copyright © © 2020 The Authors. Food Science & Nutrition published by Wiley Periodicals LLC.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 18 December 2019
                Date revision received : 14 May 2020
                Date accepted : 22 May 2020
                Page count
                Figures: 10, Tables: 1, Pages: 11, Words: 5272
                Funding
                Funded by: JSPS KAKENHI
                Award ID: JP 24500987
                Award ID: JP15K00832
                Categories
                Subject: Original Research
                Subject: Original Research
                Custom metadata
                source-schema-version-number 2.0
                cover-date July 2020
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.5 mode:remove_FC converted:25.07.2020

                Keywords: camp‐pka pathway,ethanol‐induced liver injury,hepatic stellate cells,mallotus furetianus extract,nadph oxidase,reactive oxygen species
                Data availability:
                Keywords: camp‐pka pathway, ethanol‐induced liver injury, hepatic stellate cells, mallotus furetianus extract, nadph oxidase, reactive oxygen species

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