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1.
In the present work, potential protective effects of quercitrin (a phytoestrogen) on Aβ-induced neurotoxicity in cultured
rat hippocampal neurons were investigated in comparison with 17β-estradiol. Cell viability, oxidative status, and antioxidative
potentials were used as comparative parameters. Co-exposure of cultured neurons to Aβ25–35 with either quercitrin or 17β-estradiol (50–100 μM) for 72 h attenuated Aβ25–35-induced neurotoxicity and lipid peroxidation, but not Aβ25–35-induced ROS accumulation. However, only 17β-estradiol counteracted a reduction in glutathione content and only quercitrin
counteracted a reduction in glutathione peroxidase activity. Both compounds displayed no effects on superoxide dismutase activity.
A specific estrogen receptor antagonist, ICI 182780, did not abolish neuroprotective effects of quercitrin and 17β-estradiol.
These findings suggested that quercitrin and 17β-estradiol attenuated Aβ25–35-induced neurotoxicity in a comparable manner. Underlying neuroprotective mechanisms of both compounds were probably not related
to estrogen receptor-mediated genomic mechanisms but might involve with their antioxidant and free radical scavenging properties. 相似文献
2.
In mitochondria, oxidative phosphorylation and enzymatic oxidation of biogenic amines by monoamine oxidase produce reactive
oxygen and nitrogen species, which are proposed to cause neuronal cell death in neurodegenerative disorders, including Parkinson’s
and Alzheimer’s disease. In these disorders, mitochondrial dysfunction, increased oxidative stress, and accumulation of oxidation-modified
proteins are involved in cell death in definite neurons. The interactions among these factors were studied by use of a peroxynitrite-generating
agent, N-morpholino sydnonimine (SIN-1) and an inhibitor of complex I, rotenone, in human dopaminergic SH-SY5Y cells. In control cells,
peroxynitrite nitrated proteins, especially the subunits of mitochondrial complex I, as 3-nitrotyrosine, suggesting that neurons
are exposed to constant oxidative stress even under physiological conditions. SIN-1 and an inhibitor of proteasome, carbobenzoxy-l-isoleucyl-γ-t-butyl-l-analyl-l-leucinal (PSI), increased markedly the levels of nitrated proteins with concomitant induction of apoptosis in the cells.
Rotenone induced mitochondrial dysfunction and accumulation and aggregation of proteins modified with acrolein, an aldehyde
product of lipid peroxidation in the cells. At the same time, the activity of the 20S β-subunit of proteasome was reduced
significantly, which degrades oxidative-modified protein. The mechanism was proved to be the result of the modification of
the 20S β-subunit with acrolein and to the binding of other acrolein-modified proteins to the 20S β-subunit.
Increased oxidative stress caused by SIN-1 treatment induced a decline in the mitochondrial membrane potential, ΔΨm, and activated
mitochondrial apoptotic signaling and induced cell death in SH-SY5Y cells. As another pathway, p38 mitogen-activated protein
(MAP) kinase and exracellular signal-regulated kinase (ERK) mediated apoptosis induced by SIN-1. On the other hand, a series
of neuroprotective propargylamine derivatives, including rasagiline [N-propargyl-1(R)aminoindan]and (−)deprenyl, intervened in the activation of apoptotic cascade by reactive oxygen species-reactive nitrogen
species in mitochondria through stabilization of the membrane potential, ΔΨm. In addition, rasagiline induced antiapoptotic
Bcl-2 and glial cell line-derived neurotrophic factor (GDNF) in SH-SY5Y cells, which was mediated by the ERK-nuclear factor
(NF)-κB pathway. These results are discussed in relation to the interaction of oxidative stress and mitochondria in the regulation
of neuronal death and survival in neurodegenerative diseases. 相似文献
3.
Q. Yang Z.-F. Yang S.-B. Liu X.-N. Zhang Y. Hou X.-Q. Li Y.-M. Wu A.-D. Wen Ming-Gao Zhao 《Neurochemical research》2010,35(9):1353-1360
Hydroxysafflor yellow A (HSYA) is a component of the flower Carthamus tinctorius L. that elicits neuroprotective effects in vivo and in vitro. The purpose of this study was to investigate pharmacological
properties of HSYA on neurotoxicity of glutamate in primary cultured rat cortical neurons along with its possible mechanism
of action. After challenge with N-methyl-d-aspartate (NMDA, 100 μM) for 30 min, loss of cell viability and excessive apoptotic cell death were observed in
cultured cortical neurons. However, the excitotoxic neuronal death was attenuated markedly by HSYA treatment. Western blot
analysis revealed that HSYA decreased expression of Bax and rescued the balance of pro-and anti-apoptotic proteins. In addition,
HSYA significantly reversed up-regulation of NR2B-containing NMDA receptors by exposure to NMDA, while it did not affect the
expression of NR2A-containing NMDA receptors. These finding suggest that HSYA protects cortical neurons, at least partially,
from inhibiting the expression NR2B-containing NMDA receptors and by regulating Bcl-2 family. 相似文献
4.
Masaki Kikugawa Hiroyasu Tsutsuki Tomoaki Ida Hidemitsu Nakajima Hideshi Ihara 《Bioscience, biotechnology, and biochemistry》2016,80(3):547-553
Ferulic acid (FA) has been reported to exhibit protective effects against amyloid-β (Aβ)-induced neurodegeneration in vitro and in vivo. Recently, we developed two water-soluble FA derivatives: 1-feruloyl glycerol and 1-feruloyl diglycerol. In this study, we examined the neuroprotective effects of these water-soluble FA derivatives on Aβ-induced neurodegeneration both in vitro and in vivo. FA and water-soluble FA derivatives inhibited Aβ aggregation and destabilized pre-aggregated Aβ to a similar extent. Furthermore, water-soluble FA derivatives, as well as FA, inhibited Aβ-induced neuronal cell death in cultured neuronal cells. In in vivo experiments, oral administration of water-soluble FA derivatives to mice improved Aβ-induced dysmnesia assessed by contextual fear conditioning test and protected hippocampal neurons against Aβ-induced neurotoxicity. This study provides useful evidence suggesting that water-soluble FA derivatives are expected to be effective neuroprotective agents. 相似文献
5.
Polysaccharides from Wolfberry Antagonizes Glutamate Excitotoxicity in Rat Cortical Neurons 总被引:1,自引:0,他引:1
Yuen-Shan Ho Man-Shan Yu Suet-Yi Yik Kwok-Fai So Wai-Hung Yuen Raymond Chuen-Chung Chang 《Cellular and molecular neurobiology》2009,29(8):1233-1244
Glutamate excitotoxicity is involved in many neurodegenerative diseases including Alzheimer’s disease (AD). Attenuation of
glutamate toxicity is one of the therapeutic strategies for AD. Wolfberry (Lycium barbarum) is a common ingredient in oriental cuisines. A number of studies suggest that wolfberry has anti-aging properties. In recent
years, there is a trend of using dried Wolfberry as food supplement and health product in UK and North America. Previously,
we have demonstrated that a fraction of polysaccharide from Wolfberry (LBA) provided remarkable neuroprotective effects against
beta-amyloid peptide-induced cytotoxicity in primary cultures of rat cortical neurons. To investigate whether LBA can protect
neurons from other pathological factors such as glutamate found in Alzheimer brain, we examined whether it can prevent neurotoxicity
elicited by glutamate in primary cultured neurons. The glutamate-induced cell death as detected by lactate dehydrogenase assay
and caspase-3-like activity assay was significantly reduced by LBA at concentrations ranging from 10 to 500 μg/ml. Protective
effects of LBA were comparable to memantine, a non-competitive NMDA receptor antagonist. LBA provided neuroprotection even
1 h after exposure to glutamate. In addition to glutamate, LBA attenuated N-methyl-d-aspartate (NMDA)-induced neuronal damage. To further explore whether LBA might function as antioxidant, we used hydrogen
peroxide (H2O2) as oxidative stress inducer in this study. LBA could not attenuate the toxicity of H2O2. Furthermore, LBA did not attenuate glutamate-induced oxidation by using NBT assay. Western blot analysis indicated that
glutamate-induced phosphorylation of c-jun N-terminal kinase (JNK) was reduced by treatment with LBA. Taken together, LBA
exerted significant neuroprotective effects on cultured cortical neurons exposed to glutamate. 相似文献
6.
7.
Juliana Bello Baron Maurer Adaucto Bellarmino Pereira-Netto Filomena Angela Pettolino Yolanda Maria Gaspar Antony Bacic 《Trees - Structure and Function》2010,24(2):391-398
Arabinogalactan-proteins (AGPs) are a family of highly glycosylated hydroxyproline-rich glycoproteins implicated in several
aspects of plant growth and development. (β-d-glucosyl)3 Yariv phenylglycoside (β-GlcY), commonly known as Yariv reagent, selectively binds AGPs. We treated cell suspension cultures
of Araucaria
angustifolia, the Brazilian pine, with β-GlcY and observed inhibition of biomass increase in a culture medium with 50 μM β-GlcY. However,
the growth was not inhibited by (α-d-galactosyl)3 Yariv phenylglycoside (α-GalY) which does not bind AGPs. Fluorescein diacetate staining of cells indicated that β-GlcY severely
affected cell viability. However, cell swelling, bursting and release of cellular contents, all characteristics of necrotic
cell death, were not observed in β-GlcY-treated cells. Instead, programmed cell death (PCD) structural changes such as cytoplasmic
shrinkage and condensation were observed in β-GlcY-treated cells. In addition, callose accumulation, which is another marker
of PCD, was also observed in β-GlcY-treated cells. The use of both, Ac-VEID-CHO, an inhibitor of caspase-like proteolytic
activity related to PCD, and phenyl methyl sulphonyl fluoride (PMSF), a protease inhibitor known to suppress PCD, in the culture
medium did not reverse the growth inhibition caused by β-GlcY. These data indicate that the β-GlcY-induced inhibition of Araucaria cell’s growth is related to AGP perturbation, and also that this growth inhibition is due to increased cell death not driven
by necrosis. 相似文献
8.
A recombinant putative β-galactosidase from Thermoplasma acidophilum was purified as a single 57 kDa band of 82 U mg−1. The molecular mass of the native enzyme was 114 kDa as a dimer. Maximum activity was observed at pH 6.0 and 90°C. The enzyme
was unstable below pH 6.0: at pH 6 its half-life at 75°C was 28 days but at pH 4.5 was only 13 h. Catalytic efficiencies decreased
as p-nitrophenyl(pNP)-β-d-fucopyranoside (1067) > pNP-β-d-glucopyranoside (381) > pNP-β-d-galactopyranoside (18) > pNP-β-d-mannopyranoside (11 s−1 mM−1), indicating that the enzyme was a β-glycosidase. 相似文献
9.
10.
Caffeoylquinic acid (CQA) is one of the phenylpropanoids found in a variety of natural resources and foods, such as sweet
potatoes, propolis, and coffee. Previously, we reported that 3,5-di-O-caffeoylquinic acid (3,5-di-CQA) has a neuroprotective effect against amyloid-β (Aβ)-induced cell death through the overexpression
of glycolytic enzyme. Additionally, 3,5-di-CQA administration induced the improvement of spatial learning and memory on senescence
accelerated-prone mice (SAMP8). The aim of this study was to investigate whether 3,4,5-tri-O-caffeoylquinic acid (3,4,5-tri-CQA), isolated from propolis, shows a neuroprotective effect against Aβ-induced cell death
on human neuroblastoma SH-SY5Y cells. To clarify the possible mechanism, we performed proteomics and real-time RT–PCR as well
as a measurement of the intracellular adenosine triphosphate (ATP) level. These results showed that 3,4,5-tri-CQA attenuated
the cytotoxicity and prevented Aβ-mediated apoptosis. Glycolytic enzymes, phosphoglycerate mutase 1 (PGAM1) and glyceraldehyde-3-phosphate
dehydrogenase (G3PDH) were overexpressed in co-treated cells with both 3,4,5-tri-CQA and Aβ. The mRNA expression of PGAM1,
G3PDH, and phosphoglycerate kinase 1 (PGK1), and intracellular ATP level were also increased in 3,4,5-tri-CQA treated cells.
Taken together the findings in our study suggests that 3,4,5-tri-CQA shows a neuroprotective effect against Aβ-induced cell
death through the upregulation of glycolytic enzyme mRNA as well as ATP production activation. 相似文献
11.
GABAA channels were activated by GABA in outside-out patches from rat cultured hippocampal neurons. They were blocked by bicuculline
and potentiated by diazepam. In 109 of 190 outside-out patches, no channels were active before exposure to GABA (silent patches).
The other 81 patches showed spontaneous channel activity. In patches containing spontaneous channel activity, rapid application
of GABA rapidly activated channels. In 93 of the silent patches, channels could be activated by GABA but only after a delay
that was sometimes as long as 10 minutes. The maximum channel conductance of the channels activated after a delay increased
with GABA concentration from less than 10 pS (0.5 μm GABA) to more than 100 pS (10 mm GABA). Fitting the data with a Hill-type equation gave an EC
50 value of 33 μm and a Hill coefficient of 0.6. The channels showed outward rectification and were chloride selective. In the presence of
1 μm diazepam, the GABA EC
50 decreased to 0.2 μm but the maximum conductance was unchanged. Diazepam decreased the average latency for channel opening. Bicuculline, a GABA
antagonist, caused a concentration-dependent decrease in channel conductance. In channels activated with 100 μm GABA the bicuculline IC
50 was 19 μm. The effect of GABA on channel conductance shows that the role of the ligand in GABAA receptor channel function is more complex than previously thought.
Received: 23 October 2000/Revised: 27 February 2001 相似文献
12.
J. Rath Robert Messner Paul Kosma Friedrich Altmann Leopold März Christian P. Kubicek 《Archives of microbiology》1995,164(6):414-419
A heteroglycan responsible for the binding of the enzyme β-1,4-d-glucosidase (EC 3.2.1.21) to fungal cell walls was isolated from cell walls of the filamentous fungusTrichoderma reesei. The heteroglycan, composed of mannose, galactose, glucose, and glucuronic acid, also activated β-1,4-d-glucosidase, β-1,4-d-xylosidase andN-acetyl-β-1,4-d-glucosaminidase activity in vitro. The structural backbone of this heteroglycan was prepared by acid hydrolysis and gel filtration.
The molecular structure of the core of the heteroglycan was determined by NMR studies as a linear α-1,6-d-mannan. The mannan core obtained by acid degradation stimulated the β-glucosidase activity by 90%. Several glycosidases fromAspergillus niger were also activated by theT. reesei heteroglycan. The β-glucosidase ofTrichoderma was activated by mannan fromSaccharomyces cerevisiae to a comparable extent. 相似文献
13.
Hélio V. Nobre-Júnior Ricardo A. Oliveira Flavio D. Maia Marcelle A. S. Nogueira Manoel Odorico de Moraes Mary Anne M. Bandeira Geanne M. Andrade Glauce S. B. Viana 《Neurochemical research》2009,34(6):1066-1075
In the present work, we showed that a chalcone-enriched fraction (CEF) isolated from the stem bark of a Brazilian medicinal
plant, Myracrodruon
urundeuva, presents neuroprotective actions on 6-hydroxydopamine (6-OHDA)-induced neuronal cell death, in rat mesencephalic cells.
In the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium] assay, which is an index of cell viability, CEF (1–100 μg/ml)
reversed in a concentration-dependent manner the 6-OHDA-induced cell death. While cells exposed to 6-OHDA (40 μM) showed an
increased concentration of thiobarbituric acid reactive substances (TBARS), the pretreatment with CEF (10–100 μg/ml) significantly
decreased the 6-OHDA-induced TBARS formation, indicative of a neuroprotection against lipoperoxidation. Furthermore, the drastic
increase of nitrite levels induced by 6-OHDA, indicative of nitric oxide formation and free radicals production, was prevented
by CEF. Double staining with acridine orange/ethidium bromide showed that cultures exposed to 6-OHDA (40 and 200 μM) presented
an increase of apoptotic and necrotic cell numbers in a concentration-dependent manner. CEF (100 μg/ml) protected cells from
apoptosis and necrosis and increased number of cells presenting a normal morphology. The immunohistochemical analysis for
tyrosine hydroxylase (TH) positive neurons indicated that 6-OHDA (40 and 200 μM) caused a concentration-dependent loss of
TH+ and TH− neurons. CEF protected both cells types from 6-OHDA-induced cell death. All together, our results demonstrated
neuroprotective effects of chalcones, which are able to reduce oxidative stress and apoptotic injury caused by 6-OHDA. Our
findings suggest that chalcones could provide benefits, along with other therapies, in neurodegenerative injuries, such as
Parkinson’s disease. 相似文献
14.
Birichevskaya LL Kvach SV Sivets GG Kalinichenko EN Zinchenko AI Mikhailopulo IA 《Biotechnology letters》2007,29(4):585-591
Enzymatic 5′-monophosphorylation and 5′-phosphatidylation of a number of β-l- and β-d-nucleosides was investigated. The first reaction, catalyzed by nucleoside phosphotransferase (NPT) from Erwinia herbicola, consisted of the transfer of the phosphate residue from p-nitrophenylphosphate (p-NPP) to the 5′-hydroxyl group of nucleoside; the second was the phospholipase d (PLD)-catalyzed transphosphatidylation of l-α-lecithin with a series of β-l- and β-d-nucleosides as the phosphatidyl acceptor resulted in the formation of the respective phospholipid-nucleoside conjugates.
Some β-l-nucleosides displayed similar or even higher substrate activity compared to the β-d-enantiomers. 相似文献
15.
When α-d-GlcNAc-OC6H4NO2
-p and β-d-(6-sulfo)-GlcNAc-OC6H4NO2-p (2) were used as substrates, β-N-acetylhexosaminidase from Aspergillus oryzae transferred the β-d-(6-sulfo)-GlcNAc(unit from 2 to α-d-GlcNAc-OC6H4NO2
-p to afford β-d-(6-sulfo)-GlcNAc-(1→4)-α-d-GlcNAc-OC6H4NO2-p (3) in a yield of 94% based on the amount of donor, 2, added. β-d-(6-sulfo)-GlcNAc-(1→4)-α-d-Glc-OC6H4NO2-p (4) was obtained with α-d-Glc-OC6H4NO2
-p as acceptor in a similar manner. With a reaction mixture of 2 and β-d-GlcNAc-OC6H4NO2-p (1) in a molar ratio of 6:1, the enzyme mediated the transfer of β-d-GlcNAc from 1 to 2, affording disaccharide β-d-GlcNAc-(1→4)-β-(6-sulfo)-d-GlcNAc-OC6H4NO2-p (5) in a yield of 13% based on the amount of 1 added. 相似文献
16.
The electrochemical detection of Escherichia coli β-d-glucuronidase activity as a means of monitoring water pollution by faecal material was investigated using separate Moraxella- and Pseudomonas putida-modified glassy carbon electrodes. The former was more sensitive and selective. The Moraxella-modified biosensor was 100 times more rapid and sensitive than the spectrophotometric detection of β-d-glucuronidase activity. The experimental limit of detection of the biosensor was two c.f.u. per 100 ml polluted water sample
within 20 min. The biosensor gave a linear response to commercial β-d-glucuronidase concentration between 0.2 ng and 2 μg ml−1. The biosensor detected activity of β-d-glucuronidase from viable but non-culturable (VBNC) cells and can therefore serve as a presence or absence device for rapid
water quality monitoring. 相似文献
17.
Zhiping Zhang Xiaoming Liu Tao Wu Junhong Liu Xu Zhang Xueyun Yang Michael J. Goodheart John F. Engelhardt Yujiong Wang 《Cell biology and toxicology》2011,27(2):107-121
Lycium barbarum fruit has been used as a Chinese traditional medicine and dietary supplement for centuries. 2-O-β-d-Glucopyranosyl-l-ascorbic acid (AA-2βG), a novel stable vitamin C analog, is one of the main biologically active components of the fruit.
In this report, we investigated the cytotoxic and antiproliferative effect of AA-2βG against cancer cells in vitro and identified
the proteins with significantly differential expression in the cervical cancer cells (Hela) cultured in the presence of AA-2βG
proteomic analysis. Our results demonstrated that the cytotoxic and antiproliferative activity of AA-2βG on cancer cell lines
were in a cell type-, time-, and dose-dependent manner. Similar to vitamin C, the AA-2βG selectively induced cell death repressed
the proliferation of Hela cells by the mechanism of cell apoptosis and cell cycle arrest induced by AA-2βG through a mechanism
of stabilizing p53 protein. However, the biological activity of inhibition of cell proliferation in other malignant cancer
cell lines or primary cells were varied, as demonstrated by either moderate inhibition or slight promotion following treatment
with AA-2βG. Comparative analysis of the proteomic profiles and immunoblot analysis identified 15 proteins associated with
repressing cell apoptosis and/or stimulating cell proliferation in Hela cells that were downregulated in the presence of AA-2βG
or vitamin C. These data indicate that a mechanism of the AA-2βG and vitamin C mediated antitumor activity by downregulating
the expression of proteins involved in cell apoptosis and proliferation and consequently inducing Hela cell apoptosis and
cell cycle arrest, suggesting that AA-2βG and vitamin C may share a similar mechanism of inducing Hela cell apoptosis. These
results also suggest that the L. barbarum fruit may be a potential dietary supplement and anticancer agent aimed at the prevention and treatment of cervical cancer. 相似文献
18.
Qinru Sun Ning Jia Weixi Wang Hui JinJiehua Xu Haitao Hu 《Biochemical and biophysical research communications》2014
As one of the most important hallmarks of Alzheimer’s disease (AD), β-amyloid (Aβ) plays important roles in inducing reactive oxygen species (ROS) generation, mitochondrial dysfunction and apoptotic cell death in neurons. Curcumin extracted from the yellow pigments spice plant turmeric shows multiplied bioactivities such as antioxidant and anti-apoptosis properties in vitro and in vivo. In the present study, the neuroprotective effect of curcumin against Aβ25–35-induced cell death in cultured cortical neurons was investigated. We found that pretreatment of curcumin prevented the cultured cortical neurons from Aβ25–35-induced cell toxicity. In addition, curcumin improved mitochondrial membrane potential (ΔΨm), decreased ROS generation and inhibited apoptotic cell death in Aβ25–35 treated neurons. Furthermore, we found that application of curcumin activated the expression of SIRT1 and subsequently decreased the expression of Bax in the presence of Aβ25–35. The protective effect of curcumin was blocked by SIRT1 siRNA. Taken together, our results suggest that activation of SIRT1 is involved in the neuroprotective action of curcumin. 相似文献
19.
TheSaccharomyces cerevisiae killer toxin K1 is a secreted α/β-heterodimeric protein toxin that kills sensitive yeast cells in a receptor-mediated two-stage
process. The first step involves toxin binding to β-1,6-d-glucan-components of the outer yeast cell surface; this step is blocked in yeast mutants bearing nuclear mutations in any
of theKRE genes whose products are involved in synthesis and/or assembly of cell wall β-d-glucans. After binding to the yeast cell wall, the killer toxin is transferred to the cytoplasmic membrane, subsequently
leading to cell death by forming lethal ion channels. In an attempt to identify a secondary K1 toxin receptor at the plasma
membrane level, we mutagenized sensitive yeast strains and isolated killer-resistant (kre) mutants that were resistant as spheroplasts. Classical yeast genetics and successive back-crossings to sensitive wild-type
strain indicated that this toxin resistance is due to mutation(s) in a single chromosomal yeast gene (KRE12), renderingkrel2 mutants incapable of binding significant amounts of toxin to the membrane. Sincekrel2 mutants showed normal toxin binding to the cell wall, but markedly reduced membrane binding, we isolated and purified cytoplasmic
membranes from akrel2 mutant and from an isogenicKre12+ strain and analyzed the membrane protein patterns by 2D-electrophoresis using a combination of isoelectric focusing and SDS-PAGE.
Using this technique, three different proteins (or subunits of a single multimeric protein) were identified that were present
in much lower amounts in thekre12 mutant. A model for K1 killer toxin action is presented in which the gene product ofKRE12 functions in vivo as a K1 docking protein, facilitating toxin binding to the membrane and subsequent ion channel formation. 相似文献
20.
Chen GT Yang M Song Y Lu ZQ Zhang JQ Huang HL Wu LJ Guo DA 《Applied microbiology and biotechnology》2008,77(6):1345-1350
Preparative-scale fermentation of ginsenoside Rb1 (1) with Acremonium strictum AS 3.2058 gave three new compounds, 12β-hydroxydammar-3-one-20 (S)-O-β-d-glucopyranoside (7), 12β, 25-dihydroxydammar-(E)-20(22)-ene-3-O-β-d-glucopyranosyl-(1→2)-β-d-glucopyranoside (8), and 12β, 20 (R), 25-trihydroxydammar-3-O-β-d-glucopyranosyl-(1→2)-β-d-glucopyranoside (9), along with five known compounds, ginsenoside Rd (2), gypenoside XVII (3), ginsenoside Rg3 (4), ginsenoside F2 (5), and compound K (6). The structural elucidation of these metabolites was based primarily on one- and two-dimensional nuclear magnetic resonance
and high-resolution electron spray ionization mass spectra analyses. Among these compounds, 2–6 are also the metabolites of ginsenoside Rb1 in mammals. This result demonstrated that microbial culture parallels mammalian metabolism; therefore, A. strictum might be a useful tool for generating mammalian metabolites of related analogs of ginsenosides for complete structural identification
and for further use in pharmaceutical research in this series of compounds. In addition, the biotransformation kinetics was
also investigated. 相似文献