Vitamin D/VDR relieves mice acute visceral pain by regulating Erk phosphorylation in thalamus

ABSTRACT

Background: There is a strong link between vitamin D deficiency and chronic pain, and its underlying mechanism is still unclear. This study attempts to explore the effect of vitamin D/VDR in acute visceral pain of mice and the underlying mechanism. Methods: VDR knockout mice and its litter wild mice was treated with 1% acetic acid to induce acute visceral pain. Wild type mice were randomly divided two groups, treated with vitamin D analogues (paricalcitol, 400 ng/kg）or vehicle 4 times a week via intraperitoneal injection, and then treated with 1% acetic acid to induce acute visceral pain and normal saline as control. The degree of pain was assessed by latent period and numbers of writhing body within first 15 mins. The data was expressed as means±SD. All data was analyzed by one-way ANOVA. P<0.05 was considered as statistically significant. Results: Supplement of Vitamin D to mice relieved acute visceral pain induced by 1% acetic acid.VDR knockout mice were apt to pain and its central neurons in the hypothalamus were activated. VDR was expressed at spinal cord dorsal and medial habenular nucleus of thalamus and increased feedback after visceral pain, especially treating with paricalcitol. Vitamin D could reverse the increase of Erk phosphorylation in mice thalamus causing by acute visceral pain via enhancing the crosstalk of VDR and p-Erk. Conclusion: Vitamin D relieves the mice acute visceral pain and reduces Erk phosphorylation in thalamus via enhancing the cross talk of VDR and p-Erk.