Abstract
Reactive oxygen species (ROS) are involved in neuropathic pain, a complicated condition after nerve tissue lesion. Vitamin D appears to improve symptoms of pain and exhibits antioxidant properties. We investigated the effects of oral administration of vitamin D3, the active form of vitamin D, on nociception, the sciatic functional index (SFI), and spinal cord pro-oxidant and antioxidant markers in rats with chronic constriction injury (CCI) of the sciatic nerve, a model of neuropathic pain. Vitamin D3 (500 IU/kg per day) attenuated the CCI-induced decrease in mechanical withdrawal threshold and thermal withdrawal latency (indicators of antinociception) and SFI. The vitamin prevented increased lipid hydroperoxide levels in injured sciatic nerve without change to total antioxidant capacity (TAC). Vitamin D3 prevented increased lipid hydroperoxide, superoxide anion generation (SAG), and hydrogen peroxide (H2O2) levels in the spinal cord, which were found in rats without treatment at 7 and 28 days post-CCI. A significant negative correlation was found between mechanical threshold and SAG and between mechanical threshold and H2O2 at day 7. Vitamin D3 also prevented decreased spinal cord total thiols content. There was an increase in TAC in the spinal cord of vitamin-treated CCI rats, compared to CCI rats without treatment only at 28 days. No significant changes were found in body weight and blood parameters of hepatic and renal function. These findings demonstrated, for first time, that vitamin D modulated pro-oxidant and antioxidant markers in the spinal cord. Since antinociception occurred in parallel with oxidative changes in the spinal cord, the oxidative changes may have contributed to vitamin D-induced antinociception.
Highlights
Neuropathic pain is caused by a lesion or disease of the somatosensory nervous system, which occurs in a variety of pathological conditions including trauma, diabetes, cancer, multiple sclerosis, ischemic attack, alcoholism, spinal cord damage, and many others [1]
Vitamin D3treated constriction injury (CCI) rats showed an improvement in mechanical withdrawal threshold over vehicle-treated rats of 43% at day 4, approximately 72% at days 8 and 15, and 74% at days 22 and 29
The present study showed, for the first time, that vitamin D3-induced antinociception occurs in parallel to changes in pro-oxidant and antioxidant markers in spinal cord of CCI rats, a model of neuropathic pain
Summary
Neuropathic pain is caused by a lesion or disease of the somatosensory nervous system, which occurs in a variety of pathological conditions including trauma, diabetes, cancer, multiple sclerosis, ischemic attack, alcoholism, spinal cord damage, and many others [1]. The prevalence of this type of pain is estimated at 1.5 to 8% of the general population, but the incidence is likely to increase due to the ageing global population, higher incidence of diabetes mellitus, and increased survival from cancer after chemotherapy [1]. H2O2 was found to activate the TRPM2 channel, a calcium permeable cation channel, in dorsal root ganglia neurons of rats with neuropathic pain induced by diabetes [5]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Brazilian Journal of Medical and Biological Research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
