• Q Hu, L Fang, F Li, S Thomas, and Z Yang.
• Department of Anesthesiology, SUNY Upstate Medical University, Syracuse, USA.
• Eur J Pain. 2015 Aug 1; 19 (7): 920-8.

BackgroundIncreased apoptotic changes in the spinal cord may be responsible for the development of chronic constriction injury (CCI)-induced neuropathic pain. We previously reported the beneficial effect of hyperbaric oxygen (HBO) in the treatment of CCI-induced neuropathic pain. In this study, we tested our hypotheses that HBO may achieve its beneficial effect by inhibiting CCI-induced proapoptosis gene expression and apoptosis in the spinal cord.MethodsMale rats were randomized into: SHAM, CCI and CCI + HBO groups. Mechanical hyperalgesia was tested daily following surgery. CCI + HBO rats were treated with HBO for 1 h daily. At 3 days post-CCI, the expression of tumour necrosis factor (TNF)-α and caspase-3 genes was detected. At 7 days post-CCI, apoptotic cells in the spinal cord were detected.ResultsThree days post-CCI, mechanical allodynia had developed in the ipsilateral paw compared with SHAM animals. HBO significantly alleviated CCI-induced mechanical allodynia. In comparison with SHAM, CCI-induced neuropathic pain was associated with higher mRNA levels of TNF-α and caspase-3. HBO significantly decreased CCI-induced mRNA levels of TNF-α and caspase-3. CCI-induced neuropathic pain was also associated with more apoptotic cells in the spinal cord 7 days post-CCI. HBO significantly reduced CCI-induced apoptosis to the level of SHAM animals.ConclusionsOverly expressed proapoptosis genes, and subsequent increase in spinal apoptotic cells, seem to contribute to the development of CCI-induced neuropathic pain. The inhibitory role of HBO on spinal proapoptosis genes and apoptotic changes may contribute to its beneficial effect on CCI-induced neuropathic pain.© 2014 European Pain Federation - EFIC®

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