Volume 14, Issue 55 (7-2007)                   RJMS 2007, 14(55): 181-190 | Back to browse issues page

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Nasirinezhad F, Ramezanian Nick E, Sadeghi M, Pazoki Torodi H. Antinociceptive effect of 1,25 Dihydroxy Vitamin D3 in a Neuropathic Pain Model. RJMS 2007; 14 (55) :181-190
URL: http://rjms.iums.ac.ir/article-1-748-en.html
Abstract:   (9401 Views)

    Background & Aim: In spite of the fact that many human beings suffer from chronic pain such as neuropathic pain the present clinical methods for treatment of neuropathic pain are not completely successful. 1,25 dihydroxy vitamin D3(1,25 Vit D3) the biologically active metabolite of vitamin D, can increase neurotrophin levels and inhibit the synthesis of nitric oxide synthase which both have potential roles in nociceptive processing. The presence of nuclear receptors of vitamin D in central nervous system indicates the role of this hormone in brain and spinal cord. Vitamin D deficiency in young people is one of the reasons of chronic pain such as musculoskeletal pain. The present experiment was conducted to identify the effects of 1,25 Vit D3 on pain behavior in neuropathic rat model. Materials and Methods: For this reason 40 male Wistar rats weighing 200-250 g were allocated to four groups each including 10 rats. A mononeuropathy was produced by chronic constrictive injury(CCI) of the sciatic nerve. 1,25 Vit D3 was administered by an i.p. injection every 2 days during a month after CCI. In order to evaluate mechanical and cold allodynia, Von frey and acetone tests were used respectively. Rats were tested before CCI, the day after CCI, and every week following CCI. For statistical comparison, ANOVA and Newman kules were used and P<0.05 was considered as significant. Results: Injection of Vitamin D in normal rats did not change pain threshold. Findings revealed the exaggerated responses in the group which received CCI. The group which was treated by 1,25 Vit D3 showed a significant reduction in responses in comparison with the other groups. Injection of Vitamin D increased cold allodynia from the first day of experiment and there was a signifficant difference between Vitamin D with vehicle group which lasted until the end of experiment. In regard to mechanical allodynia, there was a significant difference between vitamin D and the Vehicle group in the fourth week of experiment. Conclusion: Our results suggest that 1,25 dihydroxy vitamin D3 does not affect the pain threshold in normal animals but reduces abnormal pain in the rat model of neuropathy. The effect of Vitamin D on mechanical and cold allodynia came up with different initiation times and abolishes cold allodynia more effectively than mechanical allodynia. So administration of Vitamin D in clinic may provide new approach for treatment of chronic pain.

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Type of Study: Research | Subject: Human Physiology

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