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Melatonin and L-carnitin improves endothelial disfunction and oxidative stress in Type 2 diabetic rats
Vascular dysfunction is thought to play a major role in the development of diabetic cardiovascular disease. The roles of endothelial dysfunction, oxidative stress, and dyslipidemia will be considered. Melatonin as well as L-carnitine were shown to possess strong antioxidant properties. Diabetes indu...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4731948/ https://www.ncbi.nlm.nih.gov/pubmed/26803481 http://dx.doi.org/10.1016/j.redox.2015.11.007 |
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author | Salmanoglu, Derya Selcen Gurpinar, Tugba Vural, Kamil Ekerbicer, Nuran Darıverenli, Ertan Var, Ahmet |
author_facet | Salmanoglu, Derya Selcen Gurpinar, Tugba Vural, Kamil Ekerbicer, Nuran Darıverenli, Ertan Var, Ahmet |
author_sort | Salmanoglu, Derya Selcen |
collection | PubMed |
description | Vascular dysfunction is thought to play a major role in the development of diabetic cardiovascular disease. The roles of endothelial dysfunction, oxidative stress, and dyslipidemia will be considered. Melatonin as well as L-carnitine were shown to possess strong antioxidant properties. Diabetes induced with high fat diet (for 8 weeks) and multipl low doses intraperitoneal injection of STZ (twice, 30 mg/kg/d i.p). The diabetic animals were randomly assigned to one of the experimental groups as follows: Control group (C), high fat diet (HFD), STZ-induced diabetic group (HFD+STZ) , HFD+STZ diabetic group received melatonin (10 mg/kg/d i.p), HFD+STZ diabetic group received L-carnitine (0.6 g/kg/d i.p), and HFD+STZ diabetic group received glibenclamide (5 mg/kg/d, oral). The serum fasting blood glucose, insulin, total cholesterol, HDL- cholesterol, LDL-cholesterol, triglyceride and malondialdehyde (MDA) levels were tested. Acetylcholine induced endothelium-dependent relaxation and sodium nitroprusside induced endothelium-independent relaxation were measured in aortas for estimating endothelial function. Also, glutathione peroxidase (GPx), superoxide dismutase (SOD) and nitric oxide (NO) levels activities were determined in rat liver. According to our results melatonin and L-carnitine treatment decreased fasting blood glucose, total cholesterol, and LDL levels. MDA levels significantly decreased with the melatonin treatment whereas SOD levels were not significantly changed between the groups. The results suggest that especially melatonin restores the vascular responses and endothelial dysfunction in diabetes. |
format | Online Article Text |
id | pubmed-4731948 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-47319482016-02-23 Melatonin and L-carnitin improves endothelial disfunction and oxidative stress in Type 2 diabetic rats Salmanoglu, Derya Selcen Gurpinar, Tugba Vural, Kamil Ekerbicer, Nuran Darıverenli, Ertan Var, Ahmet Redox Biol Research Paper Vascular dysfunction is thought to play a major role in the development of diabetic cardiovascular disease. The roles of endothelial dysfunction, oxidative stress, and dyslipidemia will be considered. Melatonin as well as L-carnitine were shown to possess strong antioxidant properties. Diabetes induced with high fat diet (for 8 weeks) and multipl low doses intraperitoneal injection of STZ (twice, 30 mg/kg/d i.p). The diabetic animals were randomly assigned to one of the experimental groups as follows: Control group (C), high fat diet (HFD), STZ-induced diabetic group (HFD+STZ) , HFD+STZ diabetic group received melatonin (10 mg/kg/d i.p), HFD+STZ diabetic group received L-carnitine (0.6 g/kg/d i.p), and HFD+STZ diabetic group received glibenclamide (5 mg/kg/d, oral). The serum fasting blood glucose, insulin, total cholesterol, HDL- cholesterol, LDL-cholesterol, triglyceride and malondialdehyde (MDA) levels were tested. Acetylcholine induced endothelium-dependent relaxation and sodium nitroprusside induced endothelium-independent relaxation were measured in aortas for estimating endothelial function. Also, glutathione peroxidase (GPx), superoxide dismutase (SOD) and nitric oxide (NO) levels activities were determined in rat liver. According to our results melatonin and L-carnitine treatment decreased fasting blood glucose, total cholesterol, and LDL levels. MDA levels significantly decreased with the melatonin treatment whereas SOD levels were not significantly changed between the groups. The results suggest that especially melatonin restores the vascular responses and endothelial dysfunction in diabetes. Elsevier 2016-01-13 /pmc/articles/PMC4731948/ /pubmed/26803481 http://dx.doi.org/10.1016/j.redox.2015.11.007 Text en © 2015 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Research Paper Salmanoglu, Derya Selcen Gurpinar, Tugba Vural, Kamil Ekerbicer, Nuran Darıverenli, Ertan Var, Ahmet Melatonin and L-carnitin improves endothelial disfunction and oxidative stress in Type 2 diabetic rats |
title | Melatonin and L-carnitin improves endothelial disfunction and oxidative stress in Type 2 diabetic rats |
title_full | Melatonin and L-carnitin improves endothelial disfunction and oxidative stress in Type 2 diabetic rats |
title_fullStr | Melatonin and L-carnitin improves endothelial disfunction and oxidative stress in Type 2 diabetic rats |
title_full_unstemmed | Melatonin and L-carnitin improves endothelial disfunction and oxidative stress in Type 2 diabetic rats |
title_short | Melatonin and L-carnitin improves endothelial disfunction and oxidative stress in Type 2 diabetic rats |
title_sort | melatonin and l-carnitin improves endothelial disfunction and oxidative stress in type 2 diabetic rats |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4731948/ https://www.ncbi.nlm.nih.gov/pubmed/26803481 http://dx.doi.org/10.1016/j.redox.2015.11.007 |
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