The tumor-specific angiogenic activity of AITC appears to derive in part from repressing the production of nitric oxide and tumor necrosis factor-alpha. Additionally, AITC inhibits endothelial cell differentiation and proinflammatory cytokine production during angiogenesis. Recent studies even suggest that AITC inhibits metastasis of HT29 colorectal cells. Until now, however, there has been no report of an antiangiogenic effect of AITC in chronic inflammatory conditions or IBD. Based on these activities, it is reasonable to propose that the antiangiogenic activity of AITC could also significantly impact inflammation and disease pathology associated with various chronic inflammatory conditions. To evaluate this possibility, we have evaluated the prophylactic properties of AITC against Chloroquine Phosphate intestinal inflammation and angiogenesis in a mouse model of DSS-induced colitis. Several previous studies have shown that the dietary isothiocyanate AITC can significantly inhibit the growth of several types of chemically induced tumors in animal models. In addition, it has been reported that AITC can affect tumorassociated angiogenesis. To date, however, the effects of AITC on immune functions, especially angiogenesis, have not been fully characterized. Herein we have demonstrated that AITC exhibits prophylactic activity by reducing inflammation-driven angiogenesis. This could have beneficial applications in the treatment of IBD. IBD includes several idiopathic chronic inflammatory disorders of the intestine and/or colon in which patients suffer from rectal bleeding, severe diarrhea, abdominal pain, and loss of body weight. Although the processes underlying the onset of IBD are poorly understood, the pathologies defining IBD have been extensively characterized. IBD-afflicted colons are characterized by a large Danshensu number of leukocytes in the intestinal and/or colonic interstitium that result in granulomatous inflammation. Coincident with inflammatory cell infiltration is extensive transmural injury, including edema, loss of goblet cells, crypt cell hyperplasia, erosions, and ulceration. Several animal models of IBD have been developed for evaluating potential therapeutic agents. Among these, a mouse model in which colitis is established by DSS treatment is perhaps the most widely utilized. The number of genes involved in angiogenesis in this model has been shown to be quite similar to those in human ulcerative colitis, suggesting that this model can be useful for estimating the therapeutic potential of test agents for human treatment. In the present study, DSS-treated mice show symptoms characteristic of ulcerative colitis, including weight loss, shortening of the colon, and an increased DAI score. Histopathological analysis also revealed that DSS treatment results in extensive interruption of the epithelial surface, with submucosal edema and inflammatory cell infiltration that consisted of dense lymphoid aggregates devoid of germinal centers. Treatment with AITC concurrent with DSS treatment significantly ameliorates all of the symptoms associated with colitis. AITC-treated mice showed less weight loss and lower DAI scores than mice treated with only DSS. Mice treated with AITC also showed attenuated tissue injury; their colons retained a more intact epithelial surface with little inflammation. Collectively, these results suggest that AITC does attenuate DSS-induced colitis injury. Angiogenesis plays an important role in many neoplastic and chronic inflammatory disorders, including IBD.