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BACKGROUND: Konjac glucomannan (KGM) has been shown to stimulate the growth of bifidobacteria and lactobacilli in the human and rat colon. This study investigated the antioxidative effects produced after 48 h in vitro fermentation of unhydrolysed KGM and two hydrolysed KGM fractions (KH1 and KH2 with degree of polymerisation 10 and 5 respectively) by Bifidobacterium adolescentis, B. bifidum, B. breve, B. longum and Lactobacillus acidophilus respectively. The inhibitory effect on conjugated diene formation, ferric-chelating capacity, α,α-diphenyl-β-picrylhydrazyl (DPPH) radical-scavenging ability and thiobarbituric acid-reactive substances (TBARS) concentration produced by these fermentations were compared with those of oligofructose (OF) fermentation.

Dioscorea tuber phytoextracts can confer immunomodulatory activities ex vivo and improve regeneration of bone marrow cells in vivo. In present study, we evaluated specific Dioscorea phytoextracts for use ex vivo as a bone-marrow-derived dendritic cell- (DC-) based vaccine adjuvant for cancer immunotherapy. Fractionated Dioscorea extracts (DsII) were assayed for their effect on maturation and functions of DC ex vivo and antimelanoma activity of DC-based vaccine in vivo. The phytoextract from 50–75% ethanol-precipitated fraction of Dioscorea alata var. purpurea Tainung no. 5 tuber, designated as DsII-TN5, showed a strong augmentation of tumor cell lysate- (TCL-) loaded DC-mediated activation of T-cell proliferation. DsII-TN5 stimulated the expression of CD40, CD80, CD86, and IL-1β in TCL-loaded DCs and downregulated the expression of TGF-β1. DC vaccines prepared by a specific schema (TCL (2 h) + LPS (22 h)) showed the strongest antitumor activity. DsII-TN5 as a DC vaccine adjuvant showed strong antimelanoma activity and reduced myeloid-derived suppressor cell (MDSC) population in tested mice. DsII-TN5 can also activate DCs to enhance Th1- and Th17-related cytokine expressions. Biochemical analysis showed that DsII-TN5 consists mainly of polysaccharides containing a high level (53%) of mannose residues. We suggest that DsII-TN5 may have potential for future application as a potent, cost-effective adjuvant for DC-based cancer vaccines.

Chronic subcutaneous (s.c.) administration of D-galactose (DG) to BL/6J mice has been shown to induce oxidative stress and is considered a model to mimic accelerated ageing. Fructo-oligosaccharide (FO) is a well-defined prebiotic and its fermentation by lactic acid bacteria has been shown to exert antioxidative capacity. The present study was aimed to determine whether FO attenuated DG-induced oxidative stress and hepatopathy in Balb/cJ mice. Mice (12 weeks of age, n 40) were divided into control (s.c. saline), DG (s.c. 1·2 g/kg body weight), DG þ FO (5 %, w/w) and DG þ vitamin E (0·2 %, w/w) groups and were killed after 52 d of treatment. Results indicated that DG significantly decreased the hepatic superoxide dismutase and glutathione peroxidase activities. These alterations were ameliorated both by FO and vitamin E. DG increased the hepatic TAG content approximately by 7·2 % compared with the vehicle control, which was in agreement with the histological alteration. FO, similar to vitamin E, almost normalised the hepatic TAG content and ameliorated the histological characteristics of fatty liver. Similarly, the increased plasma alanine aminotransferase activity induced by DG was normalised by FO and vitamin E, respectively. Faecal bifidobacteria counts were greater in the DG þ FO and DG þ vitamin E groups compared with the DG group, respectively. In conclusion, the present study indicated that FO diminished the altered hepatic antioxidative enzyme activities and morphology caused by chronic DG administration in Balb/cJ mice, partially associated with its prebiotic role in the colon.Key words: D-Galactose: Fructo-oligosaccharide: Antioxidative capacity: Liver: Ageing One of the well-recognised ageing theories indicates that generation of oxidative stress leads to cell and tissue damage and ultimately results in ageing and cell death (1) . Chronic administration of D-galactose (DG) to BL/6J mice has been shown to induce changes which resemble accelerated ageing, such as formation of advanced glycation end products (2,3) , neurological impairment (4,5) , decreased serum antioxidative enzyme activities (4,5) and inflammation in the liver (3,6) . Several antioxidants (3,7,8) and Chinese herbs (9) have been shown to attenuate the ageing damage in C57BL/6J mice treated with DG.Fructo-oligosaccharide (FO), a well-defined prebiotic (10) , has been incorporated into drinks and desserts to improve bowel function in elderly persons (11) . Recent clinical studies have initially shown that the consumption of a prebiotic mix (12) and a FO supplement (13) beneficially reduces the blood indices of peroxidation status. However, the effect of FO in DG-induced hepatic oxidative damage has never been demonstrated.The main goal of the present study was to assess the anti-ageing and hepatoprotective effects of FO in DGadministered Balb/cJ mice, by the determination of antioxidative enzyme activities and the morphology of the liver and the biochemical indices of liver function. Materials and methods Animals and dietsMale B...

Subcutaneous (s.c.) D-galactose (DG) treatment has been shown to facilitate the development of biomarkers for Alzheimer's disease in C57BL/6J mice. The aim of the present study was to determine whether this treatment in young BALB/cJ mice, another mouse strain, enhanced oxidative stress to similar extents shown in older mice, and to further determine the effects of fructo-oligosaccharide (FO), a prebiotic fibre and vitamin E (antioxidant control) on the DG-induced oxidative damage of lipids, proteins and mitochondrial DNA, and erythrocyte antioxidant enzyme activities. Mice (12 weeks of age, n 40) were divided into four groups: vehicle (s.c. saline) þ control (modified rodent chow); DG (s.c. 1·2 g/kg body weight) þ control; DG þ FO (5 %, w/w); DG þ vitamin E (a-tocopherol, 0·2 %). Then, the animals were killed after 52 d of treatment. Another natural ageing (NA) group without any injection was killed at 47 weeks of age, which served as an aged control. The results indicated that the DG treatment enhanced malonaldehyde dimethyl acetal (MDA) levels in the plasma, liver and cerebral cortex, and protein carbonyl levels in the liver and hippocampus to similar levels shown in the NA group. FO, similar to a-tocopherol, systemically normalised DG-induced elevations in the levels of MDA in the plasma, liver and cerebral cortex, protein carbonyls in the liver and hippocampus, hepatic mitochondrial 8-oxo-deoxyguanosine and erythrocyte superoxide dismutase activity. In conclusion, the s.c. DG treatment in younger BALB/cJ mice resembled the oxidative status in older mice. FO supplementation systemically prevented DG-induced oxidative stress, probably through its fermentation products and prebiotic effect.