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Effect of Ethyl Pyruvate on Paclitaxel-Induced Neuropathic Pain in Rats
BACKGROUND: Although paclitaxel is a widely used chemotherapeutic agent for the treatment of solid cancers, side effects such as neuropathic pain lead to poor compliance and discontinuation of the therapy. Ethyl pyruvate (EP) is known to have analgesic effects in several pain models and may inhibit...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Pain Society
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3629339/ https://www.ncbi.nlm.nih.gov/pubmed/23614074 http://dx.doi.org/10.3344/kjp.2013.26.2.135 |
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author | Choi, Seong Soo Koh, Won Uk Nam, Jae Sik Shin, Jin Woo Leem, Jeong Gill Suh, Jeong Hun |
author_facet | Choi, Seong Soo Koh, Won Uk Nam, Jae Sik Shin, Jin Woo Leem, Jeong Gill Suh, Jeong Hun |
author_sort | Choi, Seong Soo |
collection | PubMed |
description | BACKGROUND: Although paclitaxel is a widely used chemotherapeutic agent for the treatment of solid cancers, side effects such as neuropathic pain lead to poor compliance and discontinuation of the therapy. Ethyl pyruvate (EP) is known to have analgesic effects in several pain models and may inhibit apoptosis. The present study was designed to investigate the analgesic effects of EP on mechanical allodynia and apoptosis in dorsal root ganglion (DRG) cells after paclitaxel administration. METHODS: Rats were randomly divided into 3 groups: 1) a control group, which received only vehicle; 2) a paclitaxel group, which received paclitaxel; and 3) an EP group, which received EP after paclitaxel administration. Mechanical allodynia was tested before and at 7 and 14 days after final paclitaxel administration. Fourteen days after paclitaxel treatment, DRG apoptosis was determined by activated caspase-3 immunoreactivity (IR). RESULTS: Post-treatment with EP did not significantly affect paclitaxel-induced allodynia, although it tended to slightly reduce sensitivities to mechanical stimuli after paclitaxel administration. After paclitaxel administration, an increase in caspase-3 IR in DRG cells was observed, which was co-localized with NF200-positive myelinated neurons. Post-treatment with EP decreased the paclitaxel-induced caspase-3 IR. Paclitaxel administration or post-treatment with EP did not alter the glial fibrillary acidic protein IRs in DRG cells. CONCLUSIONS: Inhibition of apoptosis in DRG neurons by EP may not be critical in paclitaxel-induced mechanical allodynia. |
format | Online Article Text |
id | pubmed-3629339 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | The Korean Pain Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-36293392013-04-23 Effect of Ethyl Pyruvate on Paclitaxel-Induced Neuropathic Pain in Rats Choi, Seong Soo Koh, Won Uk Nam, Jae Sik Shin, Jin Woo Leem, Jeong Gill Suh, Jeong Hun Korean J Pain Original Article BACKGROUND: Although paclitaxel is a widely used chemotherapeutic agent for the treatment of solid cancers, side effects such as neuropathic pain lead to poor compliance and discontinuation of the therapy. Ethyl pyruvate (EP) is known to have analgesic effects in several pain models and may inhibit apoptosis. The present study was designed to investigate the analgesic effects of EP on mechanical allodynia and apoptosis in dorsal root ganglion (DRG) cells after paclitaxel administration. METHODS: Rats were randomly divided into 3 groups: 1) a control group, which received only vehicle; 2) a paclitaxel group, which received paclitaxel; and 3) an EP group, which received EP after paclitaxel administration. Mechanical allodynia was tested before and at 7 and 14 days after final paclitaxel administration. Fourteen days after paclitaxel treatment, DRG apoptosis was determined by activated caspase-3 immunoreactivity (IR). RESULTS: Post-treatment with EP did not significantly affect paclitaxel-induced allodynia, although it tended to slightly reduce sensitivities to mechanical stimuli after paclitaxel administration. After paclitaxel administration, an increase in caspase-3 IR in DRG cells was observed, which was co-localized with NF200-positive myelinated neurons. Post-treatment with EP decreased the paclitaxel-induced caspase-3 IR. Paclitaxel administration or post-treatment with EP did not alter the glial fibrillary acidic protein IRs in DRG cells. CONCLUSIONS: Inhibition of apoptosis in DRG neurons by EP may not be critical in paclitaxel-induced mechanical allodynia. The Korean Pain Society 2013-04 2013-04-03 /pmc/articles/PMC3629339/ /pubmed/23614074 http://dx.doi.org/10.3344/kjp.2013.26.2.135 Text en Copyright © The Korean Pain Society, 2013 http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Choi, Seong Soo Koh, Won Uk Nam, Jae Sik Shin, Jin Woo Leem, Jeong Gill Suh, Jeong Hun Effect of Ethyl Pyruvate on Paclitaxel-Induced Neuropathic Pain in Rats |
title | Effect of Ethyl Pyruvate on Paclitaxel-Induced Neuropathic Pain in Rats |
title_full | Effect of Ethyl Pyruvate on Paclitaxel-Induced Neuropathic Pain in Rats |
title_fullStr | Effect of Ethyl Pyruvate on Paclitaxel-Induced Neuropathic Pain in Rats |
title_full_unstemmed | Effect of Ethyl Pyruvate on Paclitaxel-Induced Neuropathic Pain in Rats |
title_short | Effect of Ethyl Pyruvate on Paclitaxel-Induced Neuropathic Pain in Rats |
title_sort | effect of ethyl pyruvate on paclitaxel-induced neuropathic pain in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3629339/ https://www.ncbi.nlm.nih.gov/pubmed/23614074 http://dx.doi.org/10.3344/kjp.2013.26.2.135 |
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