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The effect of resolvin D1 on bone regeneration in a rat calvarial defect model

Resolvin D1 (RvD1) is a pro‐resolving lipid mediator of inflammation, endogenously synthesized from omega‐3 docosahexaenoic acid. The purpose of this study was to investigate the effect of RvD1 on bone regeneration using a rat calvarial defect model. Collagen 3D nanopore scaffold (COL) and Pluronic...

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Autores principales: Jiang, Xiaofeng, Liu, Jing, Li, Si, Qiu, Yingfei, Wang, Xiaoli, He, Xiaoli, Pedersen, Torbjørn Ø., Mustafa, Kamal, Xue, Ying, Mustafa, Manal, Kantarci, Alpdogan, Xing, Zhe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9804777/
https://www.ncbi.nlm.nih.gov/pubmed/35980287
http://dx.doi.org/10.1002/term.3345
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author Jiang, Xiaofeng
Liu, Jing
Li, Si
Qiu, Yingfei
Wang, Xiaoli
He, Xiaoli
Pedersen, Torbjørn Ø.
Mustafa, Kamal
Xue, Ying
Mustafa, Manal
Kantarci, Alpdogan
Xing, Zhe
author_facet Jiang, Xiaofeng
Liu, Jing
Li, Si
Qiu, Yingfei
Wang, Xiaoli
He, Xiaoli
Pedersen, Torbjørn Ø.
Mustafa, Kamal
Xue, Ying
Mustafa, Manal
Kantarci, Alpdogan
Xing, Zhe
author_sort Jiang, Xiaofeng
collection PubMed
description Resolvin D1 (RvD1) is a pro‐resolving lipid mediator of inflammation, endogenously synthesized from omega‐3 docosahexaenoic acid. The purpose of this study was to investigate the effect of RvD1 on bone regeneration using a rat calvarial defect model. Collagen 3D nanopore scaffold (COL) and Pluronic F127 hydrogel (F127) incorporated with RvD1 (RvD1‐COL‐F127 group) or COL and F127 (COL‐F127 group) were implanted in symmetrical calvarial defects. After implantation, RvD1 was administrated subcutaneously every 7 days for 4 weeks. The rats were sacrificed at weeks 1 and 8 post‐implantation. Tissue samples were analyzed by real‐time reverse transcriptase‐polymerase chain reaction and histology at week 1. Radiographical and histological analyses were done at week 8. At week 1, calvarial defects treated with RvD1 exhibited decreased numbers of inflammatory cells and tartrate‐resistant acid phosphatase (TRAP) positive cells, greater numbers of newly formed blood vessels, upregulated gene expression of vascular endothelial growth factor and alkaline phosphatase, and downregulated gene expression of receptor activator of nuclear factor‐κB ligand, interleukin‐1β and tumor necrosis factor‐α. At week 8, the radiographical results showed that osteoid area fraction of the RvD1‐COL‐F127 group was higher than that of the COL‐F127 group, and histological examination exhibited enhanced osteoid formation and newly formed blood vessels in the RvD1‐COL‐F127 group. In conclusion, this study showed that RvD1 enhanced bone formation and vascularization in rat calvarial defects.
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spelling pubmed-98047772023-01-06 The effect of resolvin D1 on bone regeneration in a rat calvarial defect model Jiang, Xiaofeng Liu, Jing Li, Si Qiu, Yingfei Wang, Xiaoli He, Xiaoli Pedersen, Torbjørn Ø. Mustafa, Kamal Xue, Ying Mustafa, Manal Kantarci, Alpdogan Xing, Zhe J Tissue Eng Regen Med Research Articles Resolvin D1 (RvD1) is a pro‐resolving lipid mediator of inflammation, endogenously synthesized from omega‐3 docosahexaenoic acid. The purpose of this study was to investigate the effect of RvD1 on bone regeneration using a rat calvarial defect model. Collagen 3D nanopore scaffold (COL) and Pluronic F127 hydrogel (F127) incorporated with RvD1 (RvD1‐COL‐F127 group) or COL and F127 (COL‐F127 group) were implanted in symmetrical calvarial defects. After implantation, RvD1 was administrated subcutaneously every 7 days for 4 weeks. The rats were sacrificed at weeks 1 and 8 post‐implantation. Tissue samples were analyzed by real‐time reverse transcriptase‐polymerase chain reaction and histology at week 1. Radiographical and histological analyses were done at week 8. At week 1, calvarial defects treated with RvD1 exhibited decreased numbers of inflammatory cells and tartrate‐resistant acid phosphatase (TRAP) positive cells, greater numbers of newly formed blood vessels, upregulated gene expression of vascular endothelial growth factor and alkaline phosphatase, and downregulated gene expression of receptor activator of nuclear factor‐κB ligand, interleukin‐1β and tumor necrosis factor‐α. At week 8, the radiographical results showed that osteoid area fraction of the RvD1‐COL‐F127 group was higher than that of the COL‐F127 group, and histological examination exhibited enhanced osteoid formation and newly formed blood vessels in the RvD1‐COL‐F127 group. In conclusion, this study showed that RvD1 enhanced bone formation and vascularization in rat calvarial defects. John Wiley and Sons Inc. 2022-08-18 2022-11 /pmc/articles/PMC9804777/ /pubmed/35980287 http://dx.doi.org/10.1002/term.3345 Text en © 2022 The Authors. Journal of Tissue Engineering and Regenerative Medicine published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Jiang, Xiaofeng
Liu, Jing
Li, Si
Qiu, Yingfei
Wang, Xiaoli
He, Xiaoli
Pedersen, Torbjørn Ø.
Mustafa, Kamal
Xue, Ying
Mustafa, Manal
Kantarci, Alpdogan
Xing, Zhe
The effect of resolvin D1 on bone regeneration in a rat calvarial defect model
title The effect of resolvin D1 on bone regeneration in a rat calvarial defect model
title_full The effect of resolvin D1 on bone regeneration in a rat calvarial defect model
title_fullStr The effect of resolvin D1 on bone regeneration in a rat calvarial defect model
title_full_unstemmed The effect of resolvin D1 on bone regeneration in a rat calvarial defect model
title_short The effect of resolvin D1 on bone regeneration in a rat calvarial defect model
title_sort effect of resolvin d1 on bone regeneration in a rat calvarial defect model
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9804777/
https://www.ncbi.nlm.nih.gov/pubmed/35980287
http://dx.doi.org/10.1002/term.3345
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