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CBS-Induced H(2)S Generation in Hippocampus Inhibits EA-Induced Analgesia

Hydrogen sulfide (H(2)S) is an important mediator participating in both physiological and pathological systems and related to the inflammatory process. Acupuncture has a therapeutic effect on inflammatory pain. However, whether H(2)S generated in the central nervous system (CNS) is a mediator of ele...

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Autores principales: Ren, Wen-Jing, Fu, Jia, Yin, Hai-Yan, Xu, Neng-Gui, Tang, Chun-Zhi, Liu, Li-Zhou, Yu, Shu-Guang, Tang, Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7210538/
https://www.ncbi.nlm.nih.gov/pubmed/32419814
http://dx.doi.org/10.1155/2020/5917910
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author Ren, Wen-Jing
Fu, Jia
Yin, Hai-Yan
Xu, Neng-Gui
Tang, Chun-Zhi
Liu, Li-Zhou
Yu, Shu-Guang
Tang, Yong
author_facet Ren, Wen-Jing
Fu, Jia
Yin, Hai-Yan
Xu, Neng-Gui
Tang, Chun-Zhi
Liu, Li-Zhou
Yu, Shu-Guang
Tang, Yong
author_sort Ren, Wen-Jing
collection PubMed
description Hydrogen sulfide (H(2)S) is an important mediator participating in both physiological and pathological systems and related to the inflammatory process. Acupuncture has a therapeutic effect on inflammatory pain. However, whether H(2)S generated in the central nervous system (CNS) is a mediator of electroacupuncture (EA) treatment for inflammatory pain is unknown. We injected complete Freund's adjuvant (CFA) to induce inflammatory pain and applied EA treatment as an interventional strategy for pain relief. The results presented here show that S-adenosyl-l-methionine (SAM), an allosteric activator of cystathionine-β-synthetase (CBS), may reverse the therapeutic effect of EA. CBS-induced H(2)S generation might get involved in the mechanism of EA-induced analgesia in the hippocampus on chronic inflammatory pain.
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spelling pubmed-72105382020-05-15 CBS-Induced H(2)S Generation in Hippocampus Inhibits EA-Induced Analgesia Ren, Wen-Jing Fu, Jia Yin, Hai-Yan Xu, Neng-Gui Tang, Chun-Zhi Liu, Li-Zhou Yu, Shu-Guang Tang, Yong Evid Based Complement Alternat Med Research Article Hydrogen sulfide (H(2)S) is an important mediator participating in both physiological and pathological systems and related to the inflammatory process. Acupuncture has a therapeutic effect on inflammatory pain. However, whether H(2)S generated in the central nervous system (CNS) is a mediator of electroacupuncture (EA) treatment for inflammatory pain is unknown. We injected complete Freund's adjuvant (CFA) to induce inflammatory pain and applied EA treatment as an interventional strategy for pain relief. The results presented here show that S-adenosyl-l-methionine (SAM), an allosteric activator of cystathionine-β-synthetase (CBS), may reverse the therapeutic effect of EA. CBS-induced H(2)S generation might get involved in the mechanism of EA-induced analgesia in the hippocampus on chronic inflammatory pain. Hindawi 2020-04-29 /pmc/articles/PMC7210538/ /pubmed/32419814 http://dx.doi.org/10.1155/2020/5917910 Text en Copyright © 2020 Wen-Jing Ren et al. http://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
Ren, Wen-Jing
Fu, Jia
Yin, Hai-Yan
Xu, Neng-Gui
Tang, Chun-Zhi
Liu, Li-Zhou
Yu, Shu-Guang
Tang, Yong
CBS-Induced H(2)S Generation in Hippocampus Inhibits EA-Induced Analgesia
title CBS-Induced H(2)S Generation in Hippocampus Inhibits EA-Induced Analgesia
title_full CBS-Induced H(2)S Generation in Hippocampus Inhibits EA-Induced Analgesia
title_fullStr CBS-Induced H(2)S Generation in Hippocampus Inhibits EA-Induced Analgesia
title_full_unstemmed CBS-Induced H(2)S Generation in Hippocampus Inhibits EA-Induced Analgesia
title_short CBS-Induced H(2)S Generation in Hippocampus Inhibits EA-Induced Analgesia
title_sort cbs-induced h(2)s generation in hippocampus inhibits ea-induced analgesia
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7210538/
https://www.ncbi.nlm.nih.gov/pubmed/32419814
http://dx.doi.org/10.1155/2020/5917910
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