Eun-Ah Bae

Transformation of ginseng saponins to ginsenoside Rh2 by acids and human intestinal bacteria and biological activities of their transformants

When ginseng water extract was incubated at 60°C in acidic conditions, its protopanaxadiol ginsenosides were transformed to ginsenoside Rg3 and ▵20-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 ▵20-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°C resepectively. The transformed ginsenoside Rg3 and ▵20-ginsenoside Rg3 were metabolized to ginsenoside Rh2 and ▵20-ginsenoside Rh2, respectively, by human fecal microflora. Among the bacteria isolated from human fecal microflora,Bacteroides sp.,Bifidobacterium sp. andFusobacterium 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 ofHelicobacter pylori.

Hepatoprotective effect of ginsenoside Rb1 and compound K on tert-butyl hydroperoxide-induced liver injury

Abstract: Background/Aim: The main component of Panax ginseng, which have been reported by many researchers, are ginsenoside Rb1, Rb2 and Rc. Orally administered ginsenosides are metabolized to 20‐O‐β‐d‐glucopyranosyl‐20(S)‐protopanaxadiol (compound K) by intestinal bacteria and absorbed to blood. To understand its hepatoprotective effect and its mechanism, the effects of ginsenoside Rb1 and its metabolite compound K on chemically injured HepG2 cells and mice were investigated.

Lactic acid bacteria inhibit proinflammatory cytokine expression and bacterial glycosaminoglycan degradation activity in dextran sulfate sodium-induced colitic mice

To evaluate the effect of lactic acid bacteria (LAB) in inflammatory bowel diseases (IBD), inhibitory effect of several LAB isolated from intestinal microflora and commercial probiotics against NO production of lipopolysaccharide (LPS)-stimulated RAW264.7 cells was measured and anti-inflammatory effect of NO production-inhibitory LAB, Lactobacillus plantarum HY115 and L. brevis HY7401, in dextran sulfate sodium (DSS)-induced experimental colitic mice was investigated. The oral administration of the LAB to mice inhibited colon shortening and myeloperoxidase productivity in DSS-induced colitic mice. These LABs repressed the mRNA expressions of IL-1beta, TNF-alpha and IFN-gamma, as well as the protein expressions of IL-1beta and IL-6 proteins in the colon. The activation of the transcription factor, NF-kB, induced by DSS, was also inhibited by LAB. The administration of LAB reduced the degradation activities of chondroitin sulfate and hyaluronic acid of intestinal bacteria, induced by DSS, of which could induce the cytotoxic metabolites against intestinal cells. These findings suggest that NO-inhibitory LAB against LPS-stimulated RAW264.7 cells may improve colitis by the regulation of the inflammatory cytokine expression via the activation of transcription factor NF-kB as well as GAGs-degrading intestinal microflora.

Antiallergic effect of the root of Paeonia lactiflora and its constituents paeoniflorin and paeonol

The root of Paeonia lactiflora PALL (PL, Family Paeoniaceae) has been used frequently as an antipyretic and anti-inflammatory agent in traditional medicines of Korea, China and Japan. To evaluate antiallergic effect of PL, we isolated its main constituents, paeoniflorin and paeonol, and evaluated in vivo their inhibitory effects against passive cutaenous anaphylaxis (PCA) reaction induced by IgE-antigen complex and scratching behaviors induced by compound 48/80. PL, paeoniflorin and paeonol potently inhibited PCA reaction and scratching behaviors in mice. Paeoniflorin exhibited the most potent inhibition against scratching behaviors and the acetic acid-induced writhing syndrome in mice. Paeonol most potently inhibited PCA reaction and mast cells degranulation. These findings suggest that PL can improve IgE-induced anaphylaxis and scratching behaviors, and may be due to the effect of its constituents, paeoniflorin and paeonol.

Protective effect of fermented red ginseng on a transient focal ischemic rats.

Red ginseng and fermented red ginseng were prepared, and their composition of ginsenosides and antiischemic effect were investigated. When ginseng was steamed at 98-100°C for 4 h and dried for 5 h at 60°C, and extracted with alcohol, its main components were ginsenoside Rg3> ginsenoside Rb1> ginsenoside Rb2. When the ginseng was suspended in water and fermented for 5 days by previously culturedBifidobacterium H-1 and freeze-dried (fermented red ginseng), its main components were compound K> ginsenoside Rg3≥ ginsenoside Rh2. Orally administered red ginseng extract did not protect ischemia-reperfusion brain injury. However, fermented red ginseng significantly protected ischemica-reperfusion brain injury. These results suggest that ginsenoside Rh2 and compound K, which was found to be at a higher content in fermented red ginseng than red ginseng, may improve ischemic brain injury.

Biotransformation of glycyrrhizin by human intestinal bacteria and its relation to biological activities.

The relationship between the metabolites of glycyrrhizin (18β-glycyrrhetinic acid-3-O-β-d-glucuronopyranosyl-(1→2)-β-d-glucuronide, GL) and their biological activities was investigated. By human intestinal microflora, GL was metabolized to 18β-glycyrrhetinic acid (GA) as a main product and to 18β-glycyrrhetinic acid-3-O-β-d-glucuronide (GAMG) as a minor product. The former reaction was catalyzed byEubacterium L-8 and the latter was byStreptococcus LJ-22. Among GL and its metabolites, GA and GAMG had more potentin vitro anti-platelet aggregation activity than GL. GA also showed the most potent cytotoxicity against tumor cell lines and the potent inhibitory activity on rotavirus infection as well as growth ofHelicobacter pylori. GAMG, the minor metabolite of GL, was the sweetest.

Dextran sulfate sodium and 2,4,6-trinitrobenzene sulfonic acid induce lipid peroxidation by the proliferation of intestinal gram-negative bacteria in mice.

AbstrectBackgroundTo understand whether TLR-4-linked NF-kB activation negatively correlates with lipid peroxidation in colitic animal models, we caused colitis by the treatment with dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzenesulfonic acid (TNBS) to C3H/HeJ (TLR-4-defective) and C3H/HeN (wild type) mice, investigated inflammatory markers, lipid peroxidation, proinflammatory cytokines and TLR-4-linked NF-κB activation, in colon and intestinal bacterial composition in vivo.MethodsOrally administered DSS and intrarectally injected TNBS all caused severe inflammation, manifested by shortened colons in both mice. These agents increased intestinal myeloperoxidase activity and the expression of the proinflammatory cytokines, IL-1β, TNF-α and IL-6, in the colon.ResultsDSS and TNBS induced the protein expression of TLR-4 and activated transcription factor NF-κB. However, these colitic agents did not express TLR-4 in C3H/HeJ mice. Of proinflammatory cytokines, IL-1β was most potently expressed in C3H/HeN mice. IL-1β potently induced NF-κB activation in CaCo-2 cells, but did not induce TLR-4 expression. DSS and TNBS increased lipid peroxide (malondialdehyde) and 4-hydroxy-2-nonenal content in the colon, but reduced glutathione content and superoxide dismutase and catalase activities. These colitic inducers increased the number of Enterobacteriaceae grown in DHL agar plates in both mice, although the number of anaerobes and bifidobacteria grown in GAM and BL agar plates was reduced. E. coli, K. pneumoniae and Proteus mirabilis isolated in DHL agar plates increased lipid peroxidation in liposomes prepared by L-α-phosphatidylcholine, but B. animalis and B. cholerium isolated from BL agar plates inhibited it.DiscussionThese findings suggest that DSS and TNBS may cause colitis by inducing lipid peroxidation and enterobacterial proliferation, which may deteriorate the colitis by regulating proinflammatory cytokines via TLR-4-linked NF-κB activation pathway.

β‐Glucuronidase inhibitor tectorigenin isolated from the flower of Pueraria thunbergiana protects carbon tetrachloride‐induced liver injury

Background/Aim: To understand the relationship between the fluctuation in serum β‐glucuronidase and hepatotoxicity, an inhibitor of β‐glucuronidase was isolated from the flowers of Pueraria thunbergiana and its hepatoprotective activity was measured.

In Vitro Anti-Helicobacterpylori activity of Panaxytriol isolated from Ginseng

This study investigated the effect that some polyacetylenes and protopanaxatriol, which were isolated from heated ginseng (family Araliaceae), have on inhibitingHelicobacter pylori (HP) growth. Among the compounds tested, panaxytriol was quite effective in inhibiting HP growth with an MIC of 50 μg/ml. Ginsenoside Rh1 and protopanaxatriol weakly inhibited H+/K+-ATPase from a rat stomach.

Bifidobacterium longum HY8004 attenuates TNBS-induced colitis by inhibiting lipid peroxidation in mice

ObjectiveTo investigate the mechanisms of the preventive activity of lactic acid bacteria in colitis, the inhibitory effect of Bifidobacterium longum HY8004, which potently inhibited lipid peroxidation in vitro, was examined in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice.MethodsWe measured the ability of lactic acid bacteria (LAB) to inhibit lipid peroxidation in vitro and to inhibit colitis outcomes, colon shortening, and myeloperoxidase activity in TNBS-induced colitis in C3H/HeN and C3H/HeJ mice. We also measured levels of the inflammatory markers interleukin (IL)-1β and tumor necrosis factor (TNF)-α and their transcription factor, NF-κB, in the colon by enzyme-linked immunosorbent assay and immunoblot analysis.ResultsAmong the LAB tested, B. logum HY8004 most potently inhibited lipid peroxidation in vitro but did not inhibit TLR-4-linked NF-κB activation in HEK cells. Oral administration of HY8004 inhibited TNBS-induced colon shortening and myeloperoxidase activity in the colon of C3H/HeN and C3H/HeJ mice as well as IL-1β and TNF-α expression. B. longum HY8004 also inhibited TNBS-induced lipid peroxidation, TLR-4 expression, and NF-κB activation in the colon of C3H/HeN and C3H/HeJ mice.ConclusionB. longum HY8004 can improve colitis via the inhibition of lipid peroxidation as well as NF-κB activation.