Feruloylated arabinoxylan (F-AX) was extracted from black wheat bran by either of two methods: ultrasonicassisted enzymatic extraction or alkaline extraction as control. The content and linkage of bound ferulic acid in the extract were investigated, and its antioxidant and in vitro digestive properties were studied. Our results showed that the enzymatic extract possessed lower relative molecular mass in a wider range when compared with the alkaline extract. They differed in monosaccharide composition and glycosidic linkage. The amount of ferulic acid in the enzymatic extract, (13.11 ± 0.19) μg/mg, was significantly higher than that of the alkaline extract, (0.05 ± 0.01) μg/mg. During the in vitro digestion of the enzymatic extract, the release of ferulic acid was very low at various digestion stages (oral: (0.06 ± 0.01) μg/mg, gastric: (0.60 ± 0.02) μg/mg, intestinal: (0.14 ± 0.01) μg/mg). In addition, the enzymatic extract possessed higher antioxidant activity than the alkaline extract. Our results provide a theoretical basis to fully preserve ferulic acid and its bioactivity during F-AX extraction from wheat bran, to explore its physiological effects, and to unleash the nutritional value of grain resources.

Ferulic acid is a widely distributed phenolic acid in plants and herbs, often conjugates with large molecules and enters the colon to exert anti-cancer effect. However, its suppression effect and mechanisms of action on colon cancer cells across various stages of Duke’s classification is not clear. This study aims to investigate the effects of ferulic acid on the migration, cell cycle, apoptosis, and signaling pathways in colon cancer cells (SW-480, Caco-2, and HCT-116) at different Duke’s stages. Results demonstrates that ferulic acid significantly inhibits the proliferation and migration of these cells, inducing cell cycle arrest at different phase, and ultimately promotes apoptosis in a dose-dependent manner. Specifically, ferulic acid activates the ATM/Chk2 and ATR/Chk1 pathways, down regulating their relative cell cycle regulatory proteins (CDK2 and Cyclin A2 complex, CDK4/6 and Cyclin D1/E1 complex), and thus leading to S-phase arrest in SW-480 and Caco-2 cells, and G1 phase arrest in HCT-116 cells, respectively. In addition, upregulated p53 and p21 proteins also contributing to the induction of apoptosis. This study is highly significant as they provide a deeper understanding of the molecular mechanisms by which ferulic acid exerts its anticancer effects at different Duke’s stages, and propose novel dietary strategy for the prevention of colon cancer.