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Prophylactic treatment with sulphonated immunoglobulin G attenuates development of mechanical allodynia-like response in mice with neuropathic pain
Human immunoglobulin G (IgG) concentrates are immune-modulating, anti-inflammatory plasma-derived products. Clinical studies in recent years have suggested that IgG attenuates neuropathic pain. In this study, effects of sulphonated IgG on the development and maintenance of a mechanical allodynia-lik...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Japanese Society of Veterinary Science
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751120/ https://www.ncbi.nlm.nih.gov/pubmed/26321444 http://dx.doi.org/10.1292/jvms.15-0195 |
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author | YAMAMOTO, Wataru ITANO, Yasuhiro KOBAYASHI, Tsunefumi MIURA, Daishiro KASAHARA, Yoshinori |
author_facet | YAMAMOTO, Wataru ITANO, Yasuhiro KOBAYASHI, Tsunefumi MIURA, Daishiro KASAHARA, Yoshinori |
author_sort | YAMAMOTO, Wataru |
collection | PubMed |
description | Human immunoglobulin G (IgG) concentrates are immune-modulating, anti-inflammatory plasma-derived products. Clinical studies in recent years have suggested that IgG attenuates neuropathic pain. In this study, effects of sulphonated IgG on the development and maintenance of a mechanical allodynia-like response were examined in mice with neuropathic pain induced by a partial sciatic nerve ligation (PSL). When sulphonated IgG (400 or 1,000 mg/kg/day, i.p.) was administered for 5 days, from 1 day before surgery to post-operative day (POD) 3, the development of a mechanical allodynia-like response was attenuated. On the other hand, sulphonated IgG had little effect on the maintenance of a mechanical allodynia-like response when administered for 5 days, from POD 11 to POD 15, at which time a mechanical allodynia-like response had already been developed. To explore the mechanism of sulphonated IgG, the mRNA expression of inflammatory cytokines was evaluated in the injured sciatic nerve. Sulphonated IgG (1,000 mg/kg/day, i.p.) that was administered for 3 days, from 1 day before surgery to POD 1, significantly attenuated the up-regulation of tumor necrosis factor-α and monocyte chemotactic protein-1 mRNAs on POD 1. These results suggest that prophylactic treatment with sulphonated IgG attenuates the development of mechanical allodynia-like response by inhibition of inflammatory cytokine expression in mice with PSL. |
format | Online Article Text |
id | pubmed-4751120 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | The Japanese Society of Veterinary Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-47511202016-02-26 Prophylactic treatment with sulphonated immunoglobulin G attenuates development of mechanical allodynia-like response in mice with neuropathic pain YAMAMOTO, Wataru ITANO, Yasuhiro KOBAYASHI, Tsunefumi MIURA, Daishiro KASAHARA, Yoshinori J Vet Med Sci Pharmacology Human immunoglobulin G (IgG) concentrates are immune-modulating, anti-inflammatory plasma-derived products. Clinical studies in recent years have suggested that IgG attenuates neuropathic pain. In this study, effects of sulphonated IgG on the development and maintenance of a mechanical allodynia-like response were examined in mice with neuropathic pain induced by a partial sciatic nerve ligation (PSL). When sulphonated IgG (400 or 1,000 mg/kg/day, i.p.) was administered for 5 days, from 1 day before surgery to post-operative day (POD) 3, the development of a mechanical allodynia-like response was attenuated. On the other hand, sulphonated IgG had little effect on the maintenance of a mechanical allodynia-like response when administered for 5 days, from POD 11 to POD 15, at which time a mechanical allodynia-like response had already been developed. To explore the mechanism of sulphonated IgG, the mRNA expression of inflammatory cytokines was evaluated in the injured sciatic nerve. Sulphonated IgG (1,000 mg/kg/day, i.p.) that was administered for 3 days, from 1 day before surgery to POD 1, significantly attenuated the up-regulation of tumor necrosis factor-α and monocyte chemotactic protein-1 mRNAs on POD 1. These results suggest that prophylactic treatment with sulphonated IgG attenuates the development of mechanical allodynia-like response by inhibition of inflammatory cytokine expression in mice with PSL. The Japanese Society of Veterinary Science 2015-08-29 2016-01 /pmc/articles/PMC4751120/ /pubmed/26321444 http://dx.doi.org/10.1292/jvms.15-0195 Text en ©2016 The Japanese Society of Veterinary Science http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. |
spellingShingle | Pharmacology YAMAMOTO, Wataru ITANO, Yasuhiro KOBAYASHI, Tsunefumi MIURA, Daishiro KASAHARA, Yoshinori Prophylactic treatment with sulphonated immunoglobulin G attenuates development of mechanical allodynia-like response in mice with neuropathic pain |
title | Prophylactic treatment with sulphonated immunoglobulin G attenuates
development of mechanical allodynia-like response in mice with neuropathic
pain |
title_full | Prophylactic treatment with sulphonated immunoglobulin G attenuates
development of mechanical allodynia-like response in mice with neuropathic
pain |
title_fullStr | Prophylactic treatment with sulphonated immunoglobulin G attenuates
development of mechanical allodynia-like response in mice with neuropathic
pain |
title_full_unstemmed | Prophylactic treatment with sulphonated immunoglobulin G attenuates
development of mechanical allodynia-like response in mice with neuropathic
pain |
title_short | Prophylactic treatment with sulphonated immunoglobulin G attenuates
development of mechanical allodynia-like response in mice with neuropathic
pain |
title_sort | prophylactic treatment with sulphonated immunoglobulin g attenuates
development of mechanical allodynia-like response in mice with neuropathic
pain |
topic | Pharmacology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751120/ https://www.ncbi.nlm.nih.gov/pubmed/26321444 http://dx.doi.org/10.1292/jvms.15-0195 |
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