Hyperbaric Oxygen Treatment Produces an Antinociceptive Response Phase and Inhibits Astrocyte Activation and Inflammatory Response in a Rat Model of Neuropathic Pain
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Hyperbaric oxygen (HBO) treatment has been proven to be a promising candidate for protection of the nervous system after acute injury in animal models of neuropathic pain. The purposes of this study were to examine the antinociceptive response phase induced by HBO treatment in a model of neuropathic pain and to determine the dependence of the treatment's mechanism of alleviating neuropathic pain on the inhibition of spinal astrocyte activation. Neuropathic pain was induced in rats by chronic constriction injury of the sciatic nerve. Mechanical threshold and thermal latency were tested preoperatively and for 1 week postoperatively, four times daily at fixed time points. Methane dicarboxylic aldehyde (MDA) and superoxide dismutase (SOD) parameters were used as indices of oxidative stress response and tested before and after the treatment. The inflammatory cytokines interleukin (IL)-1β and IL-10 were assayed in the sciatic nerve were with enzyme-linked immunoassay. Glial fibrillary acidic protein activation in the spinal cord was evaluated immunohistochemically. The rats exhibited temporary allodynia immediately after HBO treatment completion. This transient allodynia was closely associated with changes in MDA and SOD levels. A single HBO treatment caused a short-acting antinociceptive response phase. Repetitive HBO treatment led to a long-acting antinociceptive response phase and inhibited astrocyte activation. These results indicated that HBO treatment played a dual role in the aggravation and alleviation of neuropathic pain, though the aggravated pain effect (transient allodynia) was far less pronounced than the antinociceptive phase. Astrocyte inhibition and anti-inflammation may contribute to the antinociceptive effect of HBO treatment after nerve injury.
KeywordsHyperbaric oxygen Neuropathic pain Antinociception Astrocyte Chronic constriction injury
Tumor necrosis factor
Chronic constriction injury
Atmospheres absolute pressure
Mechanical withdrawal threshold
Thermal withdrawal latency
Glial fibrillary acidic protein
cAMP response element-binding protein
Methane dicarboxylic aldehyde
This work was supported by the Science and Technology Plan Project and B. Braun Anesthesia Scientific Research Fund (grant no. F10-205-1-41 and BBF 2012-012). We thank Dr. Cui Jian-Jun for supporting this study.
Conflict of Interest
There are no ethical/legal conflicts involved in the article.
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