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Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS
OBJECTIVE: Diabetes mellitus causes a decrease in cardiac output, arterial blood pressure, and heart rate. In this study, we aimed to investigate, at the molecular level, the effect of nitric oxide synthase (NOS) on heart pathology in type 1 diabetes and look at the therapeutic effect of pentoxifyll...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Kare Publishing
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5336777/ https://www.ncbi.nlm.nih.gov/pubmed/26488377 http://dx.doi.org/10.5152/akd.2015.6252 |
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author | Karabulut, Derya Ulusoy, Hasan Basri Kaymak, Emin Sönmez, Mehmet Fatih |
author_facet | Karabulut, Derya Ulusoy, Hasan Basri Kaymak, Emin Sönmez, Mehmet Fatih |
author_sort | Karabulut, Derya |
collection | PubMed |
description | OBJECTIVE: Diabetes mellitus causes a decrease in cardiac output, arterial blood pressure, and heart rate. In this study, we aimed to investigate, at the molecular level, the effect of nitric oxide synthase (NOS) on heart pathology in type 1 diabetes and look at the therapeutic effect of pentoxifylline on this pathology. METHODS: In this experimental study, 50 Wistar albino male rats were used. The rats were divided into 5 groups: group C, control; group D, only diabetes; group D+PI and D+PII, diabetes + pentoxifylline; group P, only pentoxifylline. Group D+PI rats received 50 mg/kg/day pentoxifylline over two months. However, group D+PII rats received saline in the first month and 50 mg/kg/day of pentoxifylline over the following month. At the end of two months, NOS expressions in heart tissue were assessed through immunohistochemistry analysis. The data were compared by one-way ANOVA. RESULTS: At the end of the experiments, there was increased cytoplasmic vacuolization, myofibrillar loss, cytoplasmic eosinophilia, and degeneration of cardiomyocytes; nNOS and iNOS expressions in group D decreased compared with that in group C. In group D+PI and group D+PII, nNOS and iNOS expressions improved compared with group D. CONCLUSION: As a result, we found that diabetes, a known chronic disease, causes serious damage in heart tissue. NOS plays a role in this damage, and pentoxifylline aided in improving nNOS and iNOS expression in this damage. |
format | Online Article Text |
id | pubmed-5336777 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Kare Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-53367772017-06-28 Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS Karabulut, Derya Ulusoy, Hasan Basri Kaymak, Emin Sönmez, Mehmet Fatih Anatol J Cardiol Original Investigation OBJECTIVE: Diabetes mellitus causes a decrease in cardiac output, arterial blood pressure, and heart rate. In this study, we aimed to investigate, at the molecular level, the effect of nitric oxide synthase (NOS) on heart pathology in type 1 diabetes and look at the therapeutic effect of pentoxifylline on this pathology. METHODS: In this experimental study, 50 Wistar albino male rats were used. The rats were divided into 5 groups: group C, control; group D, only diabetes; group D+PI and D+PII, diabetes + pentoxifylline; group P, only pentoxifylline. Group D+PI rats received 50 mg/kg/day pentoxifylline over two months. However, group D+PII rats received saline in the first month and 50 mg/kg/day of pentoxifylline over the following month. At the end of two months, NOS expressions in heart tissue were assessed through immunohistochemistry analysis. The data were compared by one-way ANOVA. RESULTS: At the end of the experiments, there was increased cytoplasmic vacuolization, myofibrillar loss, cytoplasmic eosinophilia, and degeneration of cardiomyocytes; nNOS and iNOS expressions in group D decreased compared with that in group C. In group D+PI and group D+PII, nNOS and iNOS expressions improved compared with group D. CONCLUSION: As a result, we found that diabetes, a known chronic disease, causes serious damage in heart tissue. NOS plays a role in this damage, and pentoxifylline aided in improving nNOS and iNOS expression in this damage. Kare Publishing 2016-05 2015-05-05 /pmc/articles/PMC5336777/ /pubmed/26488377 http://dx.doi.org/10.5152/akd.2015.6252 Text en Copyright © 2016 Turkish Society of Cardiology http://creativecommons.org/licenses/by-nc-sa/4.0 This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License |
spellingShingle | Original Investigation Karabulut, Derya Ulusoy, Hasan Basri Kaymak, Emin Sönmez, Mehmet Fatih Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS |
title | Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS |
title_full | Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS |
title_fullStr | Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS |
title_full_unstemmed | Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS |
title_short | Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS |
title_sort | therapeutic effects of pentoxifylline on diabetic heart tissue via nos |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5336777/ https://www.ncbi.nlm.nih.gov/pubmed/26488377 http://dx.doi.org/10.5152/akd.2015.6252 |
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