Vitamin D Deficiency Alters Anti-Inflammatory and Antioxidant Status in Dextran Sulfate Sodium Induced Ulcerative Colitis in Mice

Abstract

Numerous studies have implicated vitamin D deficiency in the etiology of ulcerative colitis (UC). However, no research has determined whether vitamin D deficiency is a causative factor or a consequence of UC. The purpose of this study was to determine whether vitamin D deficiency is a risk factor for the development of UC.
Methods: Mature male mice were grouped into control, ND+DSS group fed normal diet and 2.5% DSS in their water from day 21 to 28 to induce UC. DD+PC and DD+PC+DSS groups were given vitamin D deficient diet daily and paricalcitol intraperitoneally at 2 days interval for 12 days to induce vitamin D deficiency. They also received 2.5% DSS in their water from day 21 to 28 to induce UC. Disease activity index (DAI), vitamin D concentration, catalase (CAT), reduced glutathione (GSH) and superoxide dismutase (SOD), nitric oxide (NO), myeloperoxidase activity (MPO), tumor necrosis factor alpha (TNF α) and nuclear factor kappa b (NF-KB) were all estimated.
Results:The results from this study indicates that vitamin D deficiency significantly increased the disease activity index in mice exposed to DSS compared to mice with normal levels of vitamin D. Antioxidant markers including CAT GSH and SOD were all significantly lower in vitamin D-deficient mice compared to mice with normal levels of vitamin D. Inflammatory markers, such as NO, MPO, TNF α, and NF-KB, were significantly higher in vitamin D-deficient UC mice compared to mice with normal levels of vitamin D. The exacerbation of UC progression, as evident by a significant increase in inflammation and oxidative stress, is a testament to the important role that vitamin D plays.
Conclusions: The results show that the disease progression was faster in mice with vitamin D deficiency compared to mice with normal levels of vitamin D. It can be concluded that vitamin D deficiency may be a contributory predisposing factor to the development of UC.