Background: Increased 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.

Methods: Male 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.

Results: Three 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.

Conclusions: Overly 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.