天然花色苷矢车菊素-3,5-O-双葡萄糖苷具有抗氧化、抗炎和抗动脉粥样硬化功效。激活肠上皮细胞中芳香烃受体(AhR)，抑制NLRP3小体活化能缓解IBD患者的肠道慢性炎症。抑制TGF-β1/Samds通路活化可改善慢性炎症致IBD肠纤维化。富含矢车菊素-3,5-O-双葡萄糖苷的紫菜薹总花色苷提取物可激活肠上皮细胞内AhR，抑制IBD小鼠肠道NLRP3小体活化，降低肠纤维化发生。我们推测，与黄酮类AhR激动剂结构相似的矢车菊素-3,5-O-双葡萄糖苷对肠纤维化发生起干预作用。而矢车菊素-3,5-O-双葡萄糖苷调控IBD肠纤维化的研究报道较少。本研究拟利用肠成纤维细胞和IL-10基因敲除(IL-10-/-)小鼠自发IBD模型，基于AhR-NLRP3-TGF-β1/Samds轴探究矢车菊素-3,5-O-双葡萄糖调控IBD肠纤维化的分子机制，为其日后的人类IBD肠纤维化临床研究提供科学依据。

Cyanidin-3,5-O-diglucoside is natural anthocyanin with antioxidant, anti-inflammatory and anti-atherosclerosis activities. Both activation of aryl hydrocarbon receptor (AhR) in intestinal epithelial cells and inhibition of NLRP3 inflammasome were able to alleviate chronic intestinal inflammation in inflammatory bowel disease (IBD) patients. Reduction of the TGF-β1/Samds pathway was able to attenuate the intestinal fibrosis induced by chronic inflammation of IBD. Cyanidin-3,5-O-diglucoside enriched purple Brassica Campestris total anthocyanin extracts exhibited an activity to activate AhR in intestinal epithelial cells, inhibited the intestinal NLRP3 activation and reduced the intestinal fibrosis in IBD mice. We hypothesized that the cyanidin-3,5-O-diglucoside which with a structure similar to the flavonoid AhR agonists, may interfere with the development of intestinal fibrosis. However, there are few reports on the regulation of IBD intestinal fibrosis by cyanidin-3,5-O-diglucoside. The aim of the present study was to investigate the molecular mechanism of cyanidin-3,5-O-diglucoside regulate the intestinal fibrosis in IBD based on AhR-NLRP3-TGF-β1/Samds axis. The results from this study will provide some scientific evidences for preventing the intestinal fibrosis of human IBD in clinic.