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The human intestinal contains rich and diverse microbiota that utilizes a variety of polysaccharides. The intestinal microflora extends the metabolic functions of the body, obtaining energy from indigestible dietary polysaccharides. It is not only a highly competitive environment but also a comprehensive collaboration for these polysaccharides, as the microbiota work to maximize the energy harvested from them through the intestine. Indigestible dietary polysaccharides help to manage colon health and host health by affecting the gut microbial population. These polysaccharides also influence the metabolic activity of the intestinal microbiota by stimulating the formation of SCFAs. Most of these metabolic activities affect host physiology because the epithelium absorbs secondary metabolites and end products or transports them to the liver, where they could exert other beneficial effects. This article reviews the carbohydrates existing in the human intestine, the regulating actions of indigestible polysaccharides on intestinal microflora, and the molecular basis of the degradation process of these polysaccharides. Practical applications: Large deals of researches have shown that indigestible polysaccharides possess an outstanding regulation effect on the intestinal microflora, which indicates that indigestible polysaccharides have the potential to be used as prebiotics in the functional food and pharmaceutical industries. However, it is not clear how gut microbiota metabolizes these dietary polysaccharides, and how the resulting gut metabolites may further affect the intestinal microflora population and metabolism. This paper reviews the indigestible dietary polysaccharides existing in the human intestine, the regulation of polysaccharides on gut microbiota, and the molecular basis of the degradation process of these polysaccharides. This review helps to better understand the relationship between indigestible dietary polysaccharides and intestinal microflora, which will provide powerful evidence for the potential use of these polysaccharides as functional foods. [ABSTRACT FROM AUTHOR]

Su Yang Decoction (SYD) is a popular healthcare product comprised of various brassicaceous vegetables known to exhibit anticancer activity. However, the effects of SYD on tumor growth, following its combination with brassicaceous vegetables into a compound formula, require further investigation. In the present study, a quality control of SYD was subjected to high-performance liquid chromatography for the quantitative and qualitative determination of sulforaphane, the main anticancer component of SYD. SYD inhibited colon cancer cell proliferation in a dose- and time-dependent manner and induced G1 phase arrest in colon cancer HT-29 cell lines. In addition, SYD triggered caspase-mediated apoptosis in a dose-dependent manner and induced the cleavage of poly (ADP-ribose) polymerase, tumor necrosis factor superfamily member 10, X-linked inhibitor of apoptosis, and truncated BH3 interacting domain death agonist. Furthermore, the expression of FADD-like interleukin-1β-converting enzyme (FLICE)-like inhibitory proteins (FLIPs) and long isoform of FLICE-inhibitory protein was reduced by SYD and the direct targeting of cellular-FLIP with small interfering RNA inhibited colon cancer cell proliferation and decreased the SYD concentration required for proliferation inhibition. SYD treatment was also associated with the translocation of proapoptotic BCL2 associated X, apoptosis regulator to the mitochondria and the release of cytochrome c from the mitochondria to the cytosol. The aforementioned results indicate that SYD exerts anti-colorectal cancer effects through an underlying mechanism that may involve caspase activation. [ABSTRACT FROM AUTHOR]