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Hydrogen-Rich Saline Attenuated Neuropathic Pain by Reducing Oxidative Stress

Published online by Cambridge University Press:  23 September 2014

Qianbo Chen ,
Ping Chen ,
Shuangqiong Zhou ,
Xiaodi Yan ,
John Zhang ,
Xuejun Sun ,
Hongbin Yuan  and
Weifeng Yu
Qianbo Chen
Affiliation:
Department of Anesthesiology, Changzheng Hospital, Shanghai, PR China Department of Anesthesiology, Eastern Hepatobiliary Hospital, Shanghai, PR China
Ping Chen
Affiliation:
Department of Anesthesiology, Huashan Hospital, Fudan University, Shanghai, PR China
Shuangqiong Zhou
Affiliation:
Department of Anesthesiology, Changzheng Hospital, Shanghai, PR China
Xiaodi Yan
Affiliation:
Department of Anesthesiology, Changzheng Hospital, Shanghai, PR China
John Zhang
Affiliation:
Department of Neurosurgery, Loma Linda University, Loma Linda, California, United States of America
Xuejun Sun
Affiliation:
Department of Diving Medicine, Second Military Medical University, Shanghai, PR China
Hongbin Yuan*
Affiliation:
Department of Anesthesiology, Changzheng Hospital, Shanghai, PR China
Weifeng Yu*
Affiliation:
Department of Anesthesiology, Eastern Hepatobiliary Hospital, Shanghai, PR China
*
Department of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, PR China. Email: [email protected]
Department of Anesthesiology, Eastern Hepatobiliary Hospital, Second Military Medical University, Shanghai, 200433, PR China. Email:[email protected].
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Abstract

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Background:

Reactive oxygen species (ROS) are often associated with persistent pains such as neuropathic and inflammatory pain. Hydrogen gas can reduce ROS and alleviate cerebral, myocardial, and hepatic ischemia/reperfusion injuries. In the present study, we aim to investigate whether hydrogen-rich saline can reduce neuropathic pain in a rat model of chronic constriction injury (CCI).

Methods:

Thirty SD rats were randomly divided into three groups: sham group was administered sodium chloride by intrathecal injection (n=10); control groups underwent CCI surgery and were administered sodium chloride by intrathecal injection (n=10); vehicle group underwent CCI surgery and was administered hydrogen-rich saline by intrathecal injection (n=10). Drugs were administered in the dose of 100ul/kg once a day at 0.5 hours before and 1-7 day after CCI surgery. The mechanical thresholds were tested at one day before and 3-14 day after CCI surgery.

Results:

We found that hydrogen-rich saline significantly elevated the mechanical thresholds of neuropathic pain compared to vehicle (physiologic saline) control in CCI rats (p<0.05); it also decreased the levels of myeloperoxidase, maleic dialdehyde, and protein carbonyl in spinal cord by 7 days post-chronic constriction injury(p<0.05). In addition, hydrogen-rich saline also suppressed the expression of p38-mitogen-activated protein kinase (p38MAPK) and brain-derived neurotrophic factor (BDNF) in the spinal cord by 7 days post-chronic constriction injury (p<0.01, p<0.01, respectively), but had no effect on P2X4R (p>0.05), an ATP receptor.

Conclusion:

Intrathecal injection of hydrogen-rich saline can decrease oxidative stress and the expression of p38MAPK and BDNF that may contribute to the elevated threshold of neuropathic pain in rat CCI model.

Résumé

RÉSUMÉ Contexte:

Les espèces réactives oxygénées (ROS) sont souvent associées à la douleur persistante comme la douleur névropathique et la douleur inflammatoire. Le gaz hydrogène peut réduire les ROS et soulager le dommage dû à l'ischémie/la reperfusion au niveau cérébral, myocardique et hépatique. Le but de cette étude était de déterminer si le salin riche en hydrogène peut réduire la douleur névropathique chez un modèle de lésion par constriction chronique (LCC) chez le rat.

Méthode:

Trente rats SD ont été assignés au hasard à trois groupes : un groupe a subi une intervention factice et a reçu du chlorure de sodium en injection intrathécale (n = 10) ; un groupe a subi une LCC et a reçu du chlorure de sodium en injection intrathécale (n = 10) ; un groupe a subi une LCC et a reçu du salin riche en hydrogène en injection intrathécale (n = 10). Les solutions ont été administrées à la dose de 100/il/KG une fois par jour 0,5 heure avant la LCC et du jour 1 au jour 7 après l'intervention. Les seuils mécaniques ont été évalués 1 jour avant et du jour 3 au jour 14 après la LCC.

Résultats:

Nous avons constaté que le salin riche en hydrogène augmentait significativement le seuil mécanique de la douleur névropathique par rapport au témoin (le salin physiologique) chez les rats ayant subi une LCC (p ˂ 0,05). Il diminuait également les niveaux de myéloperoxydase, de dialdéhyde maléique et de protéines carbonylées dans la moelle épinière 7 jours après la LCC (p ˂ 0,05). De plus, le salin riche en hydrogène supprimait également l'expression de la protéine kinase activée par le mitogène p38 (MAPK p38) et le facteur neurotrope dérivé du cerveau (BDNF) dans la moelle épinière au 7e jour après la LCC (p ˂ 0,01 et p ˂ 0,01 respectivement), mais n'avait aucun effet sur P2X4R (p ˃ 0,05), un récepteur de l'ATP.

Conclusion:

L'injection intrathécale de salin riche en hydrogène peut diminuer le stress oxydatif et l'expression de MAPK p38 et de BDNT, ce qui pourrait contribuer à l'élévation du seuil de la douleur névropathique chez le modèle de rat ayant subi une LCC.

Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 40 , Issue 6 , November 2013 , pp. 857 - 863
Copyright
Copyright © The Canadian Journal of Neurological 2013

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