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      Effect of gamma-mangostin on testosterone levels in Leydig cell culture of Sprague-Dawley rat induced by advanced glycation end products: a preliminary study

      research-article
      Author(s): 1 , , 2 , 3
      Publication date (Electronic):
      Journal: BMC Proceedings
      Publisher: BioMed Central
      Conference name: 3rd International Symposium on Congenital Anomaly and Developmental Biology 2019 (ISCADB 2019)
      Conference date: 8-9 August 2019
      Keywords: Testosterone level, Leydig cell culture, Sprague-Dawley rat, Advanced glycation end products, Gamma-mangostin

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          Abstract

          Background

          Advanced glycation end products (AGE) is a toxic compound in the human body that can deteriorate health and induce an inflammatory response. One of the type of cells affected is Leydig cells, cells that produce testosterone and located in interstitial areas of the testes. Pericarp extract of Garcinia mangostana contains an antioxidant compound called gamma-mangostin that can decrease inflammatory responses and toxic effects of AGE. We aimed to compare the testosterone levels in Leydig cell culture of Sprague-Dawley rat induced by AGE only and following gamma-mangostin.

          Methods

          An experimental laboratory study was conducted on testosterone level in Leydig cell culture of Sprague-Dawley rats induced by advanced glycation end products 200 μg/mL and given gamma-mangostin 5 μM compared to cell cultures that were not given gamma-mangostin.

          Results

          Nine Leydig cell cultures were ascertained and divided into three groups. No significant difference was found in the testosterone level of Leydig cell culture given AGE only (1.33 ng/10 5 cells/24 h) compared to the group given AGE and gamma-mangostin (1.30 ng/10 5 cells/24 h) ( p = 0.535).

          Conclusion

          The testosterone level in Leydig cell cultures induced by AGE were lower than those not given, but similar in the AGE-only group and group given gamma-mangostin. The mean testosterone levels in all groups were in the range of expected levels (0.025–15 ng/10 5 cells/24 h). Further study with larger samples is important to clarify and confirm our findings.

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          Most cited references14

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          Epidemiology and aetiology of male infertility.

          Alan D. Irvine (1998)
          Infertility is a common problem, affecting perhaps one couple in six, the majority of whom now seek medical care. Although diagnostic problems make it difficult to establish the extent of the male partner's contribution with certainty, a number of studies suggest that male problems represent the commonest single defined cause of infertility. The World Health Organization has proposed a scheme for the diagnostic classification of male infertility, based upon a standardized approach to clinical assessment and to the assessment of semen quality. Some of these classifications are now controversial, and many are descriptive, rather than aetiological. Increasingly, the importance of occupation, environmental and particularly genetic factors in the causation of male infertility is being recognized.
          Article 0 comments Cited 120 times – based on 0 reviews     Review now
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            Advanced Glycation End Products Induce Calcification of Vascular Smooth Muscle Cells through RAGE/p38 MAPK

            Takahisa Tanikawa, Yosuke Okada, Rena Tanikawa … (2009)
            Background: Mönckeberg’s calcification in diabetes, known as medial artery calcification, is an independent predictor of cardiovascular mortality. However, the mechanism underlying this phenomenon remains to be elucidated. We demonstrate that advanced glycation end products (AGEs) induce calcification of vascular smooth muscle cells through the receptor for AGE (RAGE)/p38 mitogen-activated protein kinase (MAPK) signaling pathway. Methods: We detected vascular calcification by von Kossa staining. Alkaline phosphatase (ALP) activity was determined by measuring p -nitrophenol. Osteocalcin concentrations were measured using ELISA. Western blotting for protein phosphorylation and real-time RT-PCR for expression of mRNA were used. Results: AGEs induced calcification of vascular smooth muscle cells. AGEs also induced the expression of Runx2 mRNA. In addition, AGEs increased ALP activity and osteocalcin secretion. Furthermore, AGEs induced phosphorylation of p38 MAPK, and this phosphorylation was inhibited by the anti-RAGE blocking antibody. Increased ALP activity was inhibited by the p38 MAPK inhibitor or anti-RAGE blocking antibody. Furthermore, the p38 MAPK inhibitor and anti-RAGE blocking antibody both inhibited AGE-induced calcification of vascular smooth muscle cells. Diabetic serum induced calcification of smooth muscle cells and the calcification was inhibited by RAGE blocking. Conclusion: Our findings indicate that AGEs induce calcification of vascular smooth muscle cells by osteoblast-like differentiation of smooth muscle cells through RAGE/p38 MAPK.
            Article 0 comments Cited 64 times – based on 0 reviews     Review now
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              Leydig cell aging and the mechanisms of reduced testosterone synthesis.

              Barry Zirkin, Vassilios Papadopoulos, Haolin Chen … (2009)
              In males, serum testosterone levels decline with advancing age. Though part of a complex process, this age-related decline in testosterone appears to occur, in part, due to a significant decline in the ability of aged Leydig cells to produce testosterone maximally in response to luteinizing hormone (LH). The structure of the molecular machinery responsible for the synthesis of testosterone is described, and placed in the context of Leydig cell biology. Multiple parameters related to the synthesis of testosterone by the Leydig cell have been observed to change with age. Relationships among these changes are reviewed. A discussion of potential causes of the age-related decline in Leydig cell steroidogenic capacity presents a model in which the inability of aged cells to adequately respond to hormonal stimulation results in cellular regression with concomitant decline in maximal testosterone output.
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                Author and article information

                Contributors
                Dicky Moch Rizal: drdickyandrologi@ugm.ac.id
                Aditya Rifqi Fauzi: aditya96.mail@gmail.com
                Rustamaji: rustamajifarklin@ugm.ac.id
                Conference
                Journal ID (nlm-ta): BMC Proc
                Journal ID (iso-abbrev): BMC Proc
                Title: BMC Proceedings
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1753-6561
                Publication date (Electronic): 16 December 2019
                Publication date PMC-release: 16 December 2019
                Publication date Collection: 2019
                Volume: 13
                Issue : Suppl 11 Issue sponsor : Publication of this supplement has been supported by the Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada. The articles have undergone the journal's standard peer review process for supplements. Supplement Editors did not handle the peer review of articles that they co-authored. The Supplement Editors declare that they have no competing interests.
                Electronic Location Identifier: 12
                Affiliations
                [1 ]GRID grid.8570.a, Department of Physiology, Faculty of Medicine, , Public Health and Nursing Universitas Gadjah Mada/Dr. Sardjito Hospital, ; Yogyakarta, 55281 Indonesia
                [2 ]GRID grid.8570.a, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada/Dr. Sardjito Hospital, ; Yogyakarta, 55281 Indonesia
                [3 ]GRID grid.8570.a, Department of Pharmacology and Therapy, Faculty of Medicine, , Public Health and Nursing Universitas Gadjah Mada, /Dr. Sardjito Hospital, ; Yogyakarta, 55281 Indonesia
                Article
                Publisher ID: 173
                DOI: 10.1186/s12919-019-0173-x
                PMC ID: 6912937
                PubMed ID: 31890005
                SO-VID: a451f86c-4682-4ff3-8666-65d6549cf82e
                Copyright © © The Author(s). 2019
                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.

                Conference name: 3rd International Symposium on Congenital Anomaly and Developmental Biology 2019
                Conference acronym: ISCADB 2019
                Conference location: Yogyakarta, Indonesia
                Conference date: 8-9 August 2019
                History
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Medicine
                Keywords: testosterone level,leydig cell culture,sprague-dawley rat,advanced glycation end products,gamma-mangostin
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: testosterone level, leydig cell culture, sprague-dawley rat, advanced glycation end products, gamma-mangostin

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