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      Drug Design, Development and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the design and development of drugs, as well as the clinical outcomes, patient safety, and programs targeted at the effective and safe use of medicines. Sign up for email alerts here.

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      Glucocorticoid-Like Activity of Escin: A New Mechanism for an Old Drug

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          Abstract

          Saponins are a group of compounds used in clinical practice in the management of several diseases. Escin is a natural mixture of triterpene saponins which mainly consist of several isoforms, in which the α- and β-escin are predominant. β-escin is the major active compound that exerts a therapeutic effect by relieving tissue edema, promoting venous drainage, and reducing inflammation. In this review, we describe the features of its glucocorticoid-like activity that could explain its clinical effects. Using PubMed, Embase Cochrane library and reference lists for articles published until October 01, 2020, we documented that escin is likely able to exert its anti-inflammatory and anti-edematous effects through a glucocorticoid-like activity, but without the development of glucocorticoid-like adverse drug reactions.

          Most cited references50

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          NF-kappa B and Rel proteins: evolutionarily conserved mediators of immune responses.

          S. GHOSH, M. J. May, E Kopp (1998)
          The transcription factor NF-kappa B, more than a decade after its discovery, remains an exciting and active area of study. The involvement of NF-kappa B in the expression of numerous cytokines and adhesion molecules has supported its role as an evolutionarily conserved coordinating element in the organism's response to situations of infection, stress, and injury. Recently, significant advances have been made in elucidating the details of the pathways through which signals are transmitted to the NF-kappa B:I kappa B complex in the cytosol. The field now awaits the discovery and characterization of the kinase responsible for the inducible phosphorylation of I kappa B proteins. Another exciting development has been the demonstration that in certain situations NF-kappa B acts as an anti-apoptotic protein; therefore, elucidation of the mechanism by which NF-kappa B protects against cell death is an important goal. Finally, the generation of knockouts of members of the NF-kappa B/I kappa B family has allowed the study of the roles of these proteins in normal development and physiology. In this review, we discuss some of these recent findings and their implications for the study of NF-kappa B.
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            Selective transcription in response to an inflammatory stimulus.

            Stephen T. Smale (2010)
            An inflammatory response is initiated by the temporally controlled activation of genes encoding a broad range of regulatory and effector proteins. A central goal is to devise strategies for the selective modulation of proinflammatory gene transcription, to allow the suppression of genes responsible for inflammation-associated pathologies while maintaining a robust host response to microbial infection. Toward this goal, recent studies have revealed an unexpected level of diversity in the mechanisms by which chromatin structure and individual transcription factors contribute to the selective regulation of inflammatory genes. 2010 Elsevier Inc. All rights reserved.
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              A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death.

              Francesca D'Adamio, Ornella Zollo, Rosalba Moraca … (1997)
              By comparing mRNA species expressed in dexamethasone (DEX)-treated and untreated murine thymocytes, we have identified a gene, glucocorticoid-induced leucine zipper (GILZ), encoding a new member of the leucine zipper family. GILZ was found expressed in normal lymphocytes from thymus, spleen, and lymph nodes, whereas low or no expression was detected in other nonlymphoid tissues, including brain, kidney, and liver. In thymocytes and peripheral T cells, GILZ gene expression is induced by DEX. Furthermore, GILZ expression selectively protects T cells from apoptosis induced by treatment with anti-CD3 monoclonal antibody but not by treatment with other apoptotic stimuli. This antiapoptotic effect correlates with inhibition of Fas and Fas ligand expression. Thus, GILZ is a candidate transcription factor involved in the regulation of apoptosis of T cells.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Drug Des Devel Ther
                Journal ID (iso-abbrev): Drug Des Devel Ther
                Journal ID (publisher-id): dddt
                Journal ID (pmc): dddt
                Title: Drug Design, Development and Therapy
                Publisher: Dove
                ISSN (Electronic): 1177-8881
                Publication date (Electronic): 24 February 2021
                Publication date Collection: 2021
                Volume: 15
                Pages: 699-704
                Affiliations
                [1 ]Department of Health Science, School of Medicine, Operative Unit of Clinical Pharmacology, Mater Domini University Hospital , Catanzaro, Italy
                [2 ]Research Center FAS@UMG, University Magna Graecia of Catanzaro , Catanzaro, Italy
                [3 ]Department of Pharmacy, Health and Nutritional Sciences, Department of Excellence 2018–2022, University of Calabria , Rende, 87036, CS, Italy
                [4 ]Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, School of Pharmacy, Yantai University , Yantai, People’s Republic of China
                Author notes
                Correspondence: Luca Gallelli Department of Health Science, School of Medicine, Operative Unit of Clinical Pharmacology, Mater Domini University Hospital , Catanzaro, ItalyTel +39 0961712322 Email gallelli@unicz.it
                Leiming Zhang Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, School of Pharmacy, Yantai University , Yantai, People’s Republic of ChinaTel +86 5356706066 Email zhangleiming2009@126.com
                Author information
                http://orcid.org/0000-0003-0858-7902
                http://orcid.org/0000-0002-0562-0597
                Article
                Publisher ID: 297501
                DOI: 10.2147/DDDT.S297501
                PMC ID: 7917317
                SO-VID: 897a67aa-1758-4700-a2ea-94e19cf5b156
                Copyright © © 2021 Gallelli et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 17 December 2020
                Date accepted : 05 February 2021
                Page count
                Figures: 2, Tables: 1, References: 50, Pages: 6
                Categories
                Subject: Review

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: escin,mechanism of action,glucocorticoid-like activity,clinical efficacy
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: escin, mechanism of action, glucocorticoid-like activity, clinical efficacy

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