Abstract

To assess the ameliorating effects of vitamin D3 on inflammatory bowel disease in rats via the Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B signaling pathway. Thirty two rats were randomly assigned into Control group, model group (Vehicle group), low-concentration vitamin D3 group (vitamin D3 low group) and high-concentration vitamin D3 group (vitamin D3 high group). The model of inflammatory bowel disease was constructed using 3 % dextran sodium sulfate and given different concentrations of vitamin D3. Disease activity index score was calculated, colon tissues were pathologically scored by hematoxylin-eosin staining, and the mRNA expression levels of Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B were measured by quantitative reverse transcriptionpolymerase chain reaction. The expression levels of serum tumor necrosis factor-α, pro-inflammatory factors interleukin 1β and interleukin 6, as well as anti-inflammatory factor interleukin 10 were detected through enzyme-linked immunosorbent assay. The disease activity index score, mRNA expression levels of Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B and expression levels of tumor necrosis factor-α, interleukin 1β and interleukin 6 were significantly higher in Vehicle group than those in Control group, while the expression level of interleukin-10 was lower in Vehicle group (p<0.05). After intervention with vitamin D3, vitamin D3 low group and vitamin D3 high group had significantly decreased disease activity index score, messenger RNA expression levels of Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B and expression levels of tumor necrosis factor-α, interleukin 1β and interleukin 6, increased interleukin-10 expression level, and relieved damage of colon tissues compared with Vehicle group (p<0.05). Vitamin D3 ameliorates intestinal injury and colonic inflammation in inflammatory bowel disease rats by suppressing the Toll-like receptor 4/myeloid differential factor 88/ nuclear factor kappa B signaling pathway and decreasing the expression of downstream pro-inflammatory factors.