The effects of supplemental melatonin administration on the healing of bone defects in streptozotocin-induced diabetic rats

ABSTRACT Diabetes mellitus (DM) causes an increased production of free radicals that can impair bone healing. Melatonin is a hormone secreted mainly by the pineal gland, which participates in the neutralization process of free radicals. Objective The aim of this study was to investigate histologic...

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Main Authors: Senem YILDIRIMTURK, Sule BATU, Canan ALATLI, Vakur OLGAC, Deniz FIRAT, Yigit SIRIN
Format: Article
Language:English
Published: University of São Paulo
Series:Journal of Applied Oral Science
Subjects:
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1678-77572016000300239&lng=en&tlng=en
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author Senem YILDIRIMTURK
Sule BATU
Canan ALATLI
Vakur OLGAC
Deniz FIRAT
Yigit SIRIN
author_facet Senem YILDIRIMTURK
Sule BATU
Canan ALATLI
Vakur OLGAC
Deniz FIRAT
Yigit SIRIN
author_sort Senem YILDIRIMTURK
collection DOAJ
description ABSTRACT Diabetes mellitus (DM) causes an increased production of free radicals that can impair bone healing. Melatonin is a hormone secreted mainly by the pineal gland, which participates in the neutralization process of free radicals. Objective The aim of this study was to investigate histologic and biochemical effects of supplemental melatonin administration on bone healing and antioxidant defense mechanism in diabetic rats. Material and Methods Eighty-six Sprague-Dawley male rats were used in this study. Diabetes mellitus was induced by intraperitoneal (i.p.) administration of 65 mg/kg streptozotocin (STZ). Surgical bone defects were prepared in the tibia of each animal. Diabetic animals and those in control groups were treated either with daily melatonin (250 μg/animal/day/i.p.) diluted in ethanol, only ethanol, or sterile saline solution. Rats were humanely killed at the 10th and 30th postoperative days. Plasma levels of Advanced Oxidation Protein Products (AOPP), Malondialdehyde (MDA), and Superoxide Dismutase (SOD) were measured. The number of osteoblasts, blood vessels and the area of new mineralized tissue formation were calculated in histologic sections. Results At the 10th day, DM+MEL (rats receiving both STZ and melatonin) group had significantly higher number of osteoblasts and blood vessels as well as larger new mineralized tissue surfaces (p<0.05 for each) when compared with DM group. At the 30th day, DM group treated with melatonin had significantly lower levels of AOPP and MDA than those of DM group (p<0.05). Conclusion Melatonin administration in STZ induced diabetic rats reduced oxidative stress related biomarkers and showed beneficial effects on bone healing at short term.
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spelling doaj.art-ddd2ddad92194f40ac0eb87ca9650bbb2022-12-22T00:54:05ZengUniversity of São PauloJournal of Applied Oral Science1678-776524323924910.1590/1678-775720150570S1678-77572016000300239The effects of supplemental melatonin administration on the healing of bone defects in streptozotocin-induced diabetic ratsSenem YILDIRIMTURKSule BATUCanan ALATLIVakur OLGACDeniz FIRATYigit SIRINABSTRACT Diabetes mellitus (DM) causes an increased production of free radicals that can impair bone healing. Melatonin is a hormone secreted mainly by the pineal gland, which participates in the neutralization process of free radicals. Objective The aim of this study was to investigate histologic and biochemical effects of supplemental melatonin administration on bone healing and antioxidant defense mechanism in diabetic rats. Material and Methods Eighty-six Sprague-Dawley male rats were used in this study. Diabetes mellitus was induced by intraperitoneal (i.p.) administration of 65 mg/kg streptozotocin (STZ). Surgical bone defects were prepared in the tibia of each animal. Diabetic animals and those in control groups were treated either with daily melatonin (250 μg/animal/day/i.p.) diluted in ethanol, only ethanol, or sterile saline solution. Rats were humanely killed at the 10th and 30th postoperative days. Plasma levels of Advanced Oxidation Protein Products (AOPP), Malondialdehyde (MDA), and Superoxide Dismutase (SOD) were measured. The number of osteoblasts, blood vessels and the area of new mineralized tissue formation were calculated in histologic sections. Results At the 10th day, DM+MEL (rats receiving both STZ and melatonin) group had significantly higher number of osteoblasts and blood vessels as well as larger new mineralized tissue surfaces (p<0.05 for each) when compared with DM group. At the 30th day, DM group treated with melatonin had significantly lower levels of AOPP and MDA than those of DM group (p<0.05). Conclusion Melatonin administration in STZ induced diabetic rats reduced oxidative stress related biomarkers and showed beneficial effects on bone healing at short term.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1678-77572016000300239&lng=en&tlng=enBoneFree radicalsDiabetes mellitusMelatoninRats
spellingShingle Senem YILDIRIMTURK
Sule BATU
Canan ALATLI
Vakur OLGAC
Deniz FIRAT
Yigit SIRIN
The effects of supplemental melatonin administration on the healing of bone defects in streptozotocin-induced diabetic rats
Journal of Applied Oral Science
Bone
Free radicals
Diabetes mellitus
Melatonin
Rats
title The effects of supplemental melatonin administration on the healing of bone defects in streptozotocin-induced diabetic rats
title_full The effects of supplemental melatonin administration on the healing of bone defects in streptozotocin-induced diabetic rats
title_fullStr The effects of supplemental melatonin administration on the healing of bone defects in streptozotocin-induced diabetic rats
title_full_unstemmed The effects of supplemental melatonin administration on the healing of bone defects in streptozotocin-induced diabetic rats
title_short The effects of supplemental melatonin administration on the healing of bone defects in streptozotocin-induced diabetic rats
title_sort effects of supplemental melatonin administration on the healing of bone defects in streptozotocin induced diabetic rats
topic Bone
Free radicals
Diabetes mellitus
Melatonin
Rats
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1678-77572016000300239&lng=en&tlng=en
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