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      Tumor growth activity of duloxetine in Ehrlich carcinoma in mice

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          Abstract

          Objective

          The objective of this study was to analyze whether duloxetine influences tumor growth in Ehrlich carcinoma. The mice were administered 5 or 30 mg/kg of duloxetine or saline solution. All animals were inoculated with tumor cells. The tumor progression was evaluated by body weight, abdominal circumference, ascites volume and tumor cell count. The effect of duloxetine on immune response was evaluated by lymphoid cells, nitric oxide (NO) production, arginase and superoxide dismutase (SOD) activity and the spleen immunophenotyping.

          Results

          There was no difference between the groups regarding weight, abdominal circumference, ascites volume and number of tumor cells. Duloxetine increased the cells of the inguinal lymph node. There was no difference in the number of cells in the bone marrow and spleen. Ascites SOD activity was greater in Duloxetine groups. There were no differences in the levels of NO, nitrite, and arginase. The number of antibody for CD3 (CD3+), CD4+, CD8+ and CD28+ cells was lower in the duloxetine groups. In conclusion, duloxetine has no direct effect on tumor growth and does not alter immunity. The drug increased the SOD that fights free radicals and led the migration of lymphocytes, suggesting that duloxetine could be used in tumor-bearing individuals.

          Electronic supplementary material

          The online version of this article (10.1186/s13104-018-3655-4) contains supplementary material, which is available to authorized users.

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          Most cited references17

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          Superoxide dismutase as a target for the selective killing of cancer cells.

          P. Huang, L Feng, E Oldham … (2000)
          Superoxide dismutases (SOD) are essential enzymes that eliminate superoxide radical (O2-) and thus protect cells from damage induced by free radicals. The active O2- production and low SOD activity in cancer cells may render the malignant cells highly dependent on SOD for survival and sensitive to inhibition of SOD. Here we report that certain oestrogen derivatives selectively kill human leukaemia cells but not normal lymphocytes. Using complementary DNA microarray and biochemical approaches, we identify SOD as a target of this drug action and show that chemical modifications at the 2-carbon (2-OH, 2-OCH3) of the derivatives are essential for SOD inhibition and for apoptosis induction. Inhibition of SOD causes accumulation of cellular O2- and leads to free-radical-mediated damage to mitochondrial membranes, the release of cytochrome c from mitochondria and apoptosis of the cancer cells. Our results indicate that targeting SOD may be a promising approach to the selective killing of cancer cells, and that mechanism-based combinations of SOD inhibitors with free-radical-producing agents may have clinical applications.
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            The Potential Role of Nitric Oxide in Halting Cancer Progression Through Chemoprevention

            Huzefa Vahora, Munawwar Ali Khan, Usama Alalami … (2016)
            Nitric oxide (NO) in general plays a beneficial physiological role as a vasorelaxant and the role of NO is decided by its concentration present in physiological environments. NO either facilitates cancer-promoting characters or act as an anti-cancer agent. The dilemma in this regard still remains unanswered. This review summarizes the recent information on NO and its role in carcinogenesis and tumor progression, as well as dietary chemopreventive agents which have NO-modulating properties with safe cytotoxic profile. Understanding the molecular mechanisms and cross-talk modulating NO effect by these chemopreventive agents can allow us to develop better therapeutic strategies for cancer treatment.
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              Efficacy of duloxetine, a potent and balanced serotonergic and noradrenergic reuptake inhibitor, in inflammatory and acute pain models in rodents.

              Alexander H Shannon, Malcolm K. Jones, C. Peters (2005)
              Duloxetine, a selective but balanced serotonergic and noradrenergic reuptake inhibitor, was evaluated in the acute nociceptive pain models of tail flick and hot plate in mice and in the persistent and/or inflammatory pain models of acetic acid-induced writhing in mice, carrageenan-induced thermal hyperalgesia and mechanical allodynia in rats, and capsaicin-induced mechanical allodynia in rats. In acute pain models, duloxetine had no significant effect on response latency in the mouse tail-flick test but produced modest increases in response latencies in the mouse hot plate test. Morphine produced dose-related analgesic effects in both the mouse tail-flick and hot plate tests. In models of inflammatory and/or persistent pain, duloxetine, morphine, and ibuprofen produced dose-related decreases in acetic acid-induced writhing in mice. Duloxetine, ibuprofen, and gabapentin also produced dose-dependent reversals of both thermal hyperalgesia and mechanical allodynia produced by carrageenan in rats. In addition, both duloxetine and morphine produced a significant reduction of capsaicin-induced mechanical allodynia in rats. Duloxetine and gabapentin were without substantial effect on the Rotorod test in mice, whereas morphine and ibuprofen produced a significant impairment. Our data indicate that duloxetine may be efficacious in the treatment of persistent and/or inflammatory pain states at doses that have modest or no effect on acute nociception or motor performance.
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                Author and article information

                Contributors
                Ed Carlos Rey Moura: edcrmoura@yahoo.com.br
                Plinio da Cunha Leal: pliniocunhaleal@hotmail.com
                Izabel Cristina Portela Bogéa Serra: izabogea@uol.com.br
                Bruno de Paulo Ribeiro: brunodpr@hotmail.com
                Johnny Ramos do Nascimento: john_nyramos@yahoo.com.br
                Flavia Raquel Fernandes do Nascimento: nascimentofrf@yahoo.com.br
                Rioko Kimiko Sakata: 55 11 55764848 , rsakata@unifesp.br
                Journal
                Journal ID (nlm-ta): BMC Res Notes
                Journal ID (iso-abbrev): BMC Res Notes
                Title: BMC Research Notes
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1756-0500
                Publication date (Electronic): 31 July 2018
                Publication date PMC-release: 31 July 2018
                Publication date Collection: 2018
                Volume: 11
                Electronic Location Identifier: 525
                Affiliations
                [1 ]ISNI 0000 0001 2165 7632, GRID grid.411204.2, Universidade Federal do Maranhão, ; São Luís, Brazil
                [2 ]ISNI 0000 0001 0514 7202, GRID grid.411249.b, Universidade Federal de São Paulo, ; Rua Três de Maio 61/51, Vila Clementino, São Paulo, Brazil
                Article
                Publisher ID: 3655
                DOI: 10.1186/s13104-018-3655-4
                PMC ID: 6069801
                PubMed ID: 30064486
                SO-VID: d7a1768d-da2f-4c87-9b2b-1fc232f1d2af
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 7 June 2018
                Date accepted : 26 July 2018
                Funding
                Funded by: Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
                Award ID: 305608/2015-0
                Award Recipient :
                Categories
                Subject: Research Note
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Medicine
                Keywords: cancer,duloxetine,tumor growth
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: cancer, duloxetine, tumor growth

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