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The efficacy of Ankaferd Blood Stopper(®) in an experimental Asherman syndrome model created in rats

OBJECTIVE: Asherman syndrome (AS) is a progressive disease involving menstrual disorders, recurrent pregnancy losses, and infertility developing as a result of partial or full blockade of the uterine cavity with adhesions. AS generally develops after trauma to the basal layer of the endometrium. In...

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Autores principales: Büyük, Başak, Beyazıt, Fatma
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Galenos Publishing 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6463422/
https://www.ncbi.nlm.nih.gov/pubmed/31019834
http://dx.doi.org/10.4274/tjod.galenos.2018.21298
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author Büyük, Başak
Beyazıt, Fatma
author_facet Büyük, Başak
Beyazıt, Fatma
author_sort Büyük, Başak
collection PubMed
description OBJECTIVE: Asherman syndrome (AS) is a progressive disease involving menstrual disorders, recurrent pregnancy losses, and infertility developing as a result of partial or full blockade of the uterine cavity with adhesions. AS generally develops after trauma to the basal layer of the endometrium. In spite of a variety of methods such as adhesiolysis, inserting intrauterine devices, and administering high doses of estrogen, treatments remain insufficient. This study aimed to assess the effects of local intrauterine Ankaferd Blood Stopper (ABS) administration in inducing endometrial proliferation and building a normal endometrial layer in a rat model. MATERIALS AND METHODS: AS was induced in 30 female Wistar albino rats. The rats were randomized into three groups: Group 1: AS group Group 2: AS + serum physiologic (SP) group Group 3: AS + ABS group AS model was induced in all animals. The uterine horns were harvested after 15 days of therapy and investigated for inflammation, fibrosis, and immunohistochemical (IHC) markers. RESULTS: Compared with the other groups, fibrosis, and inflammation were significantly reduced in group 3 (chi-square, p=19.000, 0.001 and 26.365, <0.001, respectively). The IHC assessment showed that the tumor necrosis factor-α receptor levels were not different (Kruskal-Wallis H=0.091, p=0.995), but the interleukin (IL)-1β and IL-6 expression was reduced significantly in group 3 (H, p=18.706, <0.001, and 22.114, <0.001, respectively). CONCLUSION: The therapeutic effects of local administration of ABS in rats with AS model were demonstrated histopathologically and immunohistochemically. Based on these results, ABS administration in addition to the current treatments for AS may increase the treatment success and reduce the need for advanced treatment.
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spelling pubmed-64634222019-04-24 The efficacy of Ankaferd Blood Stopper(®) in an experimental Asherman syndrome model created in rats Büyük, Başak Beyazıt, Fatma Turk J Obstet Gynecol Clinical Investigation OBJECTIVE: Asherman syndrome (AS) is a progressive disease involving menstrual disorders, recurrent pregnancy losses, and infertility developing as a result of partial or full blockade of the uterine cavity with adhesions. AS generally develops after trauma to the basal layer of the endometrium. In spite of a variety of methods such as adhesiolysis, inserting intrauterine devices, and administering high doses of estrogen, treatments remain insufficient. This study aimed to assess the effects of local intrauterine Ankaferd Blood Stopper (ABS) administration in inducing endometrial proliferation and building a normal endometrial layer in a rat model. MATERIALS AND METHODS: AS was induced in 30 female Wistar albino rats. The rats were randomized into three groups: Group 1: AS group Group 2: AS + serum physiologic (SP) group Group 3: AS + ABS group AS model was induced in all animals. The uterine horns were harvested after 15 days of therapy and investigated for inflammation, fibrosis, and immunohistochemical (IHC) markers. RESULTS: Compared with the other groups, fibrosis, and inflammation were significantly reduced in group 3 (chi-square, p=19.000, 0.001 and 26.365, <0.001, respectively). The IHC assessment showed that the tumor necrosis factor-α receptor levels were not different (Kruskal-Wallis H=0.091, p=0.995), but the interleukin (IL)-1β and IL-6 expression was reduced significantly in group 3 (H, p=18.706, <0.001, and 22.114, <0.001, respectively). CONCLUSION: The therapeutic effects of local administration of ABS in rats with AS model were demonstrated histopathologically and immunohistochemically. Based on these results, ABS administration in addition to the current treatments for AS may increase the treatment success and reduce the need for advanced treatment. Galenos Publishing 2019-03 2019-03-27 /pmc/articles/PMC6463422/ /pubmed/31019834 http://dx.doi.org/10.4274/tjod.galenos.2018.21298 Text en ©Copyright 2019 by Turkish Society of Obstetrics and Gynecology | Turkish Journal of Obstetrics and Gynecology published by Galenos Publishing House. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Clinical Investigation
Büyük, Başak
Beyazıt, Fatma
The efficacy of Ankaferd Blood Stopper(®) in an experimental Asherman syndrome model created in rats
title The efficacy of Ankaferd Blood Stopper(®) in an experimental Asherman syndrome model created in rats
title_full The efficacy of Ankaferd Blood Stopper(®) in an experimental Asherman syndrome model created in rats
title_fullStr The efficacy of Ankaferd Blood Stopper(®) in an experimental Asherman syndrome model created in rats
title_full_unstemmed The efficacy of Ankaferd Blood Stopper(®) in an experimental Asherman syndrome model created in rats
title_short The efficacy of Ankaferd Blood Stopper(®) in an experimental Asherman syndrome model created in rats
title_sort efficacy of ankaferd blood stopper(®) in an experimental asherman syndrome model created in rats
topic Clinical Investigation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6463422/
https://www.ncbi.nlm.nih.gov/pubmed/31019834
http://dx.doi.org/10.4274/tjod.galenos.2018.21298
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