Flavonoid glycosides were metabolized to phenolic acids via aglycones by human intestinal microflora producing alpha-rhamnosidase, exo-beta-glucosidase, endo-beta-glucosidase and/or beta-glucuronidase. Rutin, hesperidin, naringin and poncirin were transformed to their aglycones by the bacteria producing alpha-rhamnosidase and beta-glucosidase or endo-beta-glucosidase, and baicalin, puerarin and daidzin were transformed to their aglycones by the bacteria producing beta-glucuronidase, C-glycosidase and beta-glycosidase, respectively. Anti-platelet activity and cytotoxicity of the metabolites of flavonoid glycosides by human intestinal bacteria were more effective than those of the parental compounds. 3,4-Dihydroxyphenylacetic acid and 4-hydroxyl-phenylacetic acid were more effective than rutin and quercetin on anti-platelet aggregation activity. 2,4,6-Trihydroxybenzaldehyde, quercetin and ponciretin were more effective than rutin and ponciretin on the cytotoxicity for tumor cell lines. We insist that these flavonoid glycosides should be natural prodrugs.

Most herbal medicines are orally administered and their components inevitably come into contact with intestinal microflora in the alimentary tract. These components may be transformed before they are absorbed from the gastrointestinal tract. Studies on the metabolism of herbal medicine components by human intestinal microflora are therefore of great importance in understanding their biological effects. 1,2) Among herbal medicines, ginseng (the root of Panax ginseng C.A. MEYER, Araliaceae) is frequently used in Asian countries as a traditional medicine. The major components of ginseng are ginsenosides.3,4) These ginsenosides have been reported to show various biological activities including antiinflammatory activity 5) and antitumor effects. 6,7) The pharmacological actions of these ginsenosides has been explained by the biotransformation of ginsenosides by human intestinal bacteria. [8][9][10][11][12] Transformed 20-O-b-D-glucopyranosyl-20(S)-protopanaxadiol (IH-901, compound K) from ginsenosides R b1 , R b2 and R c induces an antimetastatic or anticarcinogenic effect. [13][14][15] In addition, ginsenosides R b1 , R b2 , and R c are transformed to ginsenoside R g3 by treatment with mild acid such as stomach acid.16) Furthermore, ginsenoside R g3 is a main component of Red Ginseng.17) However, studies on the metabolism of ginsenoside R g3 by human intestinal bacteria are not complete.Therefore we investigated the human intestinal bacteria capable of metabolizing ginsenoside R g3 and its related biological activities, such as in vitro cytotoxicity and anti-Helicobacter pylori (HP) activity. MATERIALS AND METHODS Materials and Bacterial StrainsSodium thioglycolate and ascorbic acid were purchased from Sigma Chemical Co. (U.S.A.). General anaerobic medium (GAM) was purchased from Nissui Pharmaceutical Co., Ltd., (Japan). Tryptic soy broth was purchased from Difco Co. (U.S.A.). p-Nitrophenyl b-D-glucopyranoside (PNG) was purchased from Sigma (U.S.A.). The other chemicals were of analytical reagent grade.Tumor cell lines were purchased from the Korean Cell Bank. HP ATCC43504 was purchased from ATCC, HP NCTC11638 was purchased from NCTC. HP82516 and HP4 clinically isolated from Korean gastroscopic samples were used. They were inoculated onto brucella agar plates supplemented with 7% horse serum and cultured for 3 days at 37°C under microaerophilic conditions (AnaeroPak Campylo: 85% N 2 , 10% CO 2 , and 5% O 2 ). Isolation of Transformants of Ginsenoside R b1 under Mild Acidic Conditions Ginsenoside R b1 (2 g) was treated in mild acidic conditions 16) at 37°C for 2 h, as previously reported, concentrated at 60°C and extracted with n-BuOH. From this BuOH fraction, 20(S)-and 20(R)-ginsenoside R g3 were isolated according to the previous method.18) The BuOH fraction was chromatographed on a silica gel column using CHCl 3 -MeOH-H 2 O (10 : 3 : 1, lower layer) to produce D 20 -ginsenoside R g3 (0.05 g), and isomeric 20(S)-and 20(R)-ginsenoside R g3 (0.6 g). The isomeric mixture was dissolved in pyridine, and acetic anhydride...

28While the practice of rainwater harvesting (RWH) can be traced back millennia, the degree of its 29 modern implementation varies greatly across the world, often with systems that do not maximize 30 potential benefits. With a global focus, the pertinent practical, theoretical and social aspects of RWH 31 are reviewed in order to ascertain the state of the art. Avenues for future research are also identified. 32A major finding is that the degree of RWH systems implementation and the technology selection are

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Background: Ginseng (the root of Panax ginseng C.A. Meyer, Araliaceae) has been reported to possess various biological activities, including anti-inflammatory and antitumor actions. In this study, we investigated the antiallergic activity of ginsenosides isolated from ginseng. Method: We isolated ginsenosides by silica gel column chromatograghy and examined their in vitro and in vivo antiallergic effect on rat peritoneal mast cells and on IgE-induced passive cutaneous anaphylaxis (PCA) in mice. The in vitroanti-inflammatory activity of ginsenoside Rh1 (Rh1) in RAW264.7 cells was investigated. Results: Rh1 potently inhibited histamine release from rat peritoneal mast cells and the IgE-mediated PCA reaction in mice. The inhibitory activity of Rh1 (87% inhibition at 25 mg/kg) on the PCA reaction was found to be more potent than that of disodium cromoglycate (31% inhibition at 25 mg/kg); Rh1 was also found to have a membrane-stabilizing action as revealed by differential scanning calorimetry. It also inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein expression in RAW 264.7 cells, and the activation of the transcription factor, NF-ĸB, in nuclear fractions. Conclusion: The antiallergic action of Rh1 may originate from its cell membrane-stabilizing and anti-inflammatory activities, and can improve the inflammation caused by allergies.

When ginseng water extract was incubated at 60 degrees C in acidic conditions, its protopanaxadiol ginsenosides were transformed to ginsenoside Rg3 and delta20-ginsenoside Rg3. However, protopanaxadiol glycoside ginsenosides Rb1, Rb2 and Rc isolated from ginseng were mostly not transformed to ginsenoside Rg3 by the incubation in neutral condition. The transformation of these ginsenosides to ginsenoside Rg3 and delta20-ginsenoside Rg3 was increased by increasing incubation temperature and time in acidic condition: the optimal incubation time and temperature for this transformation was 5 h and 60 degrees C resepectively. The transformed ginsenoside Rg3 and delta20-ginsenoside Rg3 were metabolized to ginsenoside Rh2 and delta20-ginsenoside Rh2, respectively, by human fecal microflora. Among the bacteria isolated from human fecal microflora, Bacteroides sp., Bifidobacterium sp. and Fusobacterium sp. potently transformed ginsenoside Rg3 to ginsenoside Rh2. Acid-treated ginseng (AG) extract, fermented AG extract, ginsenoside Rh2 and protopanaxadiol showed potent cytotoxicity against tumor cell lines. AG extract, fermented AG extract and protopanaxadiol potently inhibited the growth of Helicobacter pylori.

The aim of the present study was to determine whether there is the mechanistic connection between antibacterial-dependent gut microbiota disturbance and anxiety. First, exposure of mice to ampicillin caused anxiety and colitis and increased the population of Proteobacteria, particularly Klebsiella oxytoca, in gut microbiota and fecal and blood lipopolysaccharide levels, while decreasing lactobacilli population including Lactobacillus reuteri. Next, treatments with fecal microbiota of ampicillin-treated mouse (FAP), K. oxytoca, or lipopolysaccharide isolated from K. oxytoca (KL) induced anxiety and colitis in mice and increased blood corticosterone, IL-6, and lipopolysaccharide levels. Moreover, these treatments also increased the recruitment of microglia (Iba1), monocytes (CD11b/CD45), and dendritic cells (CD11b/CD11c) to the hippocampus, as well as the population of apoptotic neuron cells (caspase-3/NeuN) in the brain. Furthermore, ampicillin, K. oxytoca, and KL induced NF-κB activation and IL-1β and TNF-α expression in the colon and brain as well as increased gut membrane permeability. Finally, oral administration of L. reuteri alleviated ampicillin-induced anxiety and colitis. These results suggest that ampicillin exposure can cause anxiety through neuro-inflammation which can be induced by monocyte/macrophage-activated gastrointestinal inflammation and elevated Proteobacteria population including K. oxytoca, while treatment with lactobacilli suppresses it.