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Natural Hirudin Increases Rat Flap Viability by Anti-Inflammation via PARs/p38/NF-κB Pathway
The present study aimed to evaluate the effect of natural hirudin on rat random skin flap viability and to determine the mechanism. Forty-eight rats were randomly divided into 2 groups. After the dorsal skin flap operation (3 cm × 10 cm in size), subcutaneous injections of 6 ATU hirudin were adminis...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4685076/ https://www.ncbi.nlm.nih.gov/pubmed/26770977 http://dx.doi.org/10.1155/2015/597264 |
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author | Peng, Liu Pan, Xinyuan Yin, Guoqian |
author_facet | Peng, Liu Pan, Xinyuan Yin, Guoqian |
author_sort | Peng, Liu |
collection | PubMed |
description | The present study aimed to evaluate the effect of natural hirudin on rat random skin flap viability and to determine the mechanism. Forty-eight rats were randomly divided into 2 groups. After the dorsal skin flap operation (3 cm × 10 cm in size), subcutaneous injections of 6 ATU hirudin were administered to group H (n = 24) every 12 h, while group C (n = 24) received an equal volume of 0.9% normal saline. Six rats from each group were euthanized 1, 2, 4, and 7 days after the operation. A full skin sample was collected from these rats to measure the p38-mitogen-activated protein kinase (p38-MAPK), phospho-p38- (Pp38-) MAPK, nuclear factor-κB (NF-κB) p65, phosphor-NF-κB (pNF-κB) p65, tumour necrosis factor- (TNF-) α, interleukin- (IL-) 6, and intercellular adhesion molecule- (ICAM-) 1 levels via western blot (WB) assays. The results showed that flap viability was significantly higher in the hirudin-treated group, which showed a reduced inflammatory response compared with the control group. The Pp38/p38, pNF-κB p65/NF-κB p65, TNF-α, IL-6, and ICAM-1 levels in the hirudin-treated group were lower than those in the control group. The results demonstrated that hirudin could improve random skin flap viability and suggested that this effect maybe occurs by blocking the thrombin/proteinase-activated receptors (PARs)/p38/NF-κB signalling pathway, thus decreasing the inflammatory response. |
format | Online Article Text |
id | pubmed-4685076 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-46850762016-01-14 Natural Hirudin Increases Rat Flap Viability by Anti-Inflammation via PARs/p38/NF-κB Pathway Peng, Liu Pan, Xinyuan Yin, Guoqian Biomed Res Int Research Article The present study aimed to evaluate the effect of natural hirudin on rat random skin flap viability and to determine the mechanism. Forty-eight rats were randomly divided into 2 groups. After the dorsal skin flap operation (3 cm × 10 cm in size), subcutaneous injections of 6 ATU hirudin were administered to group H (n = 24) every 12 h, while group C (n = 24) received an equal volume of 0.9% normal saline. Six rats from each group were euthanized 1, 2, 4, and 7 days after the operation. A full skin sample was collected from these rats to measure the p38-mitogen-activated protein kinase (p38-MAPK), phospho-p38- (Pp38-) MAPK, nuclear factor-κB (NF-κB) p65, phosphor-NF-κB (pNF-κB) p65, tumour necrosis factor- (TNF-) α, interleukin- (IL-) 6, and intercellular adhesion molecule- (ICAM-) 1 levels via western blot (WB) assays. The results showed that flap viability was significantly higher in the hirudin-treated group, which showed a reduced inflammatory response compared with the control group. The Pp38/p38, pNF-κB p65/NF-κB p65, TNF-α, IL-6, and ICAM-1 levels in the hirudin-treated group were lower than those in the control group. The results demonstrated that hirudin could improve random skin flap viability and suggested that this effect maybe occurs by blocking the thrombin/proteinase-activated receptors (PARs)/p38/NF-κB signalling pathway, thus decreasing the inflammatory response. Hindawi Publishing Corporation 2015 2015-12-07 /pmc/articles/PMC4685076/ /pubmed/26770977 http://dx.doi.org/10.1155/2015/597264 Text en Copyright © 2015 Liu Peng et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Peng, Liu Pan, Xinyuan Yin, Guoqian Natural Hirudin Increases Rat Flap Viability by Anti-Inflammation via PARs/p38/NF-κB Pathway |
title | Natural Hirudin Increases Rat Flap Viability by Anti-Inflammation via PARs/p38/NF-κB Pathway |
title_full | Natural Hirudin Increases Rat Flap Viability by Anti-Inflammation via PARs/p38/NF-κB Pathway |
title_fullStr | Natural Hirudin Increases Rat Flap Viability by Anti-Inflammation via PARs/p38/NF-κB Pathway |
title_full_unstemmed | Natural Hirudin Increases Rat Flap Viability by Anti-Inflammation via PARs/p38/NF-κB Pathway |
title_short | Natural Hirudin Increases Rat Flap Viability by Anti-Inflammation via PARs/p38/NF-κB Pathway |
title_sort | natural hirudin increases rat flap viability by anti-inflammation via pars/p38/nf-κb pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4685076/ https://www.ncbi.nlm.nih.gov/pubmed/26770977 http://dx.doi.org/10.1155/2015/597264 |
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