Abstract
Hyperbaric oxygen treatment (HBOT) has been used to reduce neuropathic pain. Melatonin and opioid receptors are involved in neuropathic pain, but it is not known if HBOT works through these pathways to achieve its antinociceptive effect. We divided anesthetized rats into two treatment and three sham groups. The two treatment groups received third-degree burns on their right hind paws, one treated in a hyperbaric chamber for a week and the other for two weeks. We evaluated the mechanical paw-withdrawal threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) opioid receptor, brain-derived neurotrophic factor (BDNF), Substance P, and calcitonin gene-related peptide (CGRP) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real-time quantitative polymerase chain reaction (RT-PCR). The group receiving one-week HBOT had increased expressions of MT1, MT2, MOR and KOR and decreased expressions of BDNF, Substance P, and CGRP. Their mechanically measured pain levels returned to normal within a week and lasted three weeks. This anti-allodynia effect lasted twice as long in those treated for two weeks. Our findings suggest that increasing the duration of HBOT can reduce burn-induced mechanical allodynia for an extended period of time in rats. The upregulation of melatonin and opioid receptors observed after one week of HBOT suggests they may be partly involved in attenuation of the mechanical allodynia. Downregulation of BDNF, substance P and CGRP may have also contributed to the overall beneficial effect of HBOT.
Highlights
Millions of people worldwide suffer from burn-induced neuropathic pain, a chronic pain state induced by burn-induced lesions or injury of the peripheral or central nervous system [1]
These findings indicate that Hyperbaric oxygen treatment (HBOT) had a dose-dependent anti-allodynia effect in hind paw skin
Our study found expressions of the melatonin and opioid receptors melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), MOR and KOR to be significantly higher in the cuneate nucleus and dorsal horns of burned rats treated with HBOT for one week compared with those in the untreated burned rats, indicating that HBOT alleviated burn-induced neuropathic pain by increasing the expressions of the melatonin receptors and opioid receptors via this pain transmission pathway
Summary
Millions of people worldwide suffer from burn-induced neuropathic pain, a chronic pain state induced by burn-induced lesions or injury of the peripheral or central nervous system [1]. No effective analgesic or other treatments have been found to adequately manage neuropathic pain. Such continuous pain causes great physical and emotional discomfort, lowering the quality of life and requires many medical resources to manage [3]. Two different studies, both in models of chronic constriction injury (CCI), have reported that HBOT effectively reduced neuropathic pain [7,8]. We previously found that HBOT could alleviate mechanical allodynia in a burn-induced neuroinflammation rat model [12]. We wondered whether an additional benefit could be achieved by extending the duration of HBOT and which pathways might be involved in HBOT’s effect on burn-induced neuropathic pain
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