Intestinal absorption of pallidifloside D are limited by P-glycoprotein in mice.

1. Pallidifloside D, a saponin glycoside constituent from the total saponins of Smilax riparia, had been proved to be very effective in hyperuricemic control. But it is poorly bioavailable after oral administration. Here, we determined the role of P-glycoprotein (P-gp) in the intestinal absorption of Pallidifloside D. 2. We found that Pallidifloside D significantly stimulated P-gp ATPase activity in vitro ATPase assay with a small EC50 value of 0.46 µM. 3. In the single-pass perfused mouse intestine model, the absorption of Pallidifloside D was not favored in the small intestine (duodenum, jejunum and ileum) with a P*w value of 0.35-0.78. By contrast, this compound was well-absorbed in the colon with a P*w value of 1.23. The P-gp inhibitors cyclosporine significantly enhanced Pallidifloside D absorption in all four intestinal segments (duodenum, jejunum, ileum and colon) and the fold change ranged from 5.5 to 15.3. Pharmacokinetic study revealed that cyclosporine increased the systemic exposure of Pallidifloside D by a 2.5-fold after oral administration. 4. These results suggest that P-gp-mediated efflux is a limiting factor for intestinal absorption of Pallidifloside D in mice.

Effects of Smilaxchinoside A and Smilaxchinoside C, two steroidal glycosides from Smilax riparia, on hyperuricemia in a mouse model.

The roots and rhizomes of Smilax riparia, called 'Niu-Wei-Cai' in traditional Chinese medicine, are believed to be effective in treating the symptoms of gout. However, the active constituents and their uricosuric mechanisms are unknown. In this study, we isolated two steroidal glycosides, named smilaxchinoside A and smilaxchinoside C, from the total saponins obtained from the ethanol extract of the roots of S. riparia. We then examined if these two compounds were effective in reducing serum uric acid levels in a hyperuricemic mouse model induced by potassium oxonate. We observed that these two steroidal glycosides possess potent uricosuric activities, and the observed effects accompanied the reduction of renal mURAT1 and the inhibition of xanthine oxidase, which contribute to the enhancement of uric acid excretion and the reduction of hyperuricemia-induced renal dysfunction. Smilaxchinoside A and smilaxchinoside C may have a clinical utility in treating gout and other medical conditions caused by hyperuricemia.

[Review on the effects of heavy metal accumulation in flowers on the mutual benefit relationship between plant and insect pollinators]. / 花部重金属积累对植物-ä¼ ç²‰æ˜†è™«äº’æƒ å ³ç³»å½±å“çš„ç ”ç©¶è¿›å±•.

The global sharp decline of pollinators is one of the hot issues concerned by ecologists, mainly driven by global climate change, land use change, habitat fragmentation and harmful substances such as pesticides brought by industrial and agricultural production. In contrast, the potential impact of soil heavy metal pollution on pollinators is lack of in-depth evaluation. Heavy metals in soil would enter plant tissues, such as flowers, etc., and be transmitted to pollinators during pollination. By affecting pollinators' behavior, they can change plant fitness for male and female. This review aimed to comprehensively sort out the status of research and existing problems, which would deepen our understanding on the ecological consequences caused by heavy metal pollution as well as the plant-animal relationship in response to environmental change. Summarizing previous researches, we reviewed findings on the pattern of heavy metal accumulation in flowers, the impacts of flower heavy metal accumulation on plant male and female fitnesses in addition to pollination behavior and the key aspects of life history of bees, to help understand the interrelationship between flower heavy metal accumulation and pollinators, and further expand the scientific understanding on the internal connection between soil heavy metal pollution and the decline of pollinators.

L-carnitine protects against nickel-induced neurotoxicity by maintaining mitochondrial function in Neuro-2a cells.

Mitochondrial dysfunction is thought to be a part of the mechanism underlying nickel-induced neurotoxicity. L-carnitine (LC), a quaternary ammonium compound biosynthesized from the amino acids lysine and methionine in all mammalian species, manifests its neuroprotective effects by improving mitochondrial energetics and function. The purpose of this study was to investigate whether LC could efficiently protect against nickel-induced neurotoxicity. Here, we exposed a mouse neuroblastoma cell line (Neuro-2a) to different concentrations of nickel chloride (NiCl2) (0.25, 0.5, 1, and 2 mM) for 24 h, or to 0.5 mM and 1 mM NiCl2 for various periods (0, 3, 6, 12, or 24 h). We found that nickel significantly increased the cell viability loss and lactate dehydrogenase (LDH) release in Neuro-2a cells. In addition, nickel exposure significantly elevated reactive oxygen species (ROS) and malondialdehyde (MDA) levels, disrupted the mitochondrial membrane potential (ΔΨ(m)), reduced adenosine-5'-triphosphate (ATP) concentrations and decreased mitochondrial DNA (mtDNA) copy numbers and mtRNA transcript levels. However, all of the cytotoxicities and mitochondrial dysfunctions that were triggered by nickel were efficiently attenuated by pretreatment with LC. These protective effects of LC may be attributable to its role in maintaining mitochondrial function in nickel-treated cells. Our results suggest that LC may have great pharmacological potential in protecting against the adverse effects of nickel in the nervous system.

Nickel exposure induces oxidative damage to mitochondrial DNA in Neuro2a cells: the neuroprotective roles of melatonin.

Recent studies suggest that oxidative stress and mitochondrial dysfunction play important roles in the neurotoxicity of nickel. Because mitochondrial DNA (mtDNA) is highly vulnerable to oxidative stress and melatonin can efficiently protect mtDNA against oxidative damage in various pathological conditions, the aims of this study were to determine whether mtDNA oxidative damage was involved in the neurotoxicity of nickel and to assay the neuroprotective effects of melatonin in mtDNA. In this study, we exposed mouse neuroblastoma cell lines (Neuro2a) to different concentrations of nickel chloride (NiCl(2), 0.125, 0.25, and 0.5 mm) for 24 hr. We found that nickel significantly increased reactive oxygen species (ROS) production and mitochondrial superoxide levels. In addition, nickel exposure increased mitochondrial 8-hydroxyguanine (8-OHdG) content and reduced mtDNA content and mtDNA transcript levels. Consistent with this finding, nickel was found to destroy mtDNA nucleoid structure and decrease protein levels of Tfam, a key protein component for nucleoid organization. However, all the oxidative damage to mtDNA induced by nickel was efficiently attenuated by melatonin pretreatment. Our results suggest that oxidative damage to mtDNA may account for the neurotoxicity of nickel. Melatonin has great pharmacological potential in protecting mtDNA against the adverse effects of nickel in the nervous system.

Acetylated anthraquinone glycosides from Cassia obtusifolia.

Three new acetylated anthraquinone glycosides (1-3) were isolated from the seed of Cassia obtusifolia, together with one parent anthraquinone glycoside (1a). Their structures were determined on the basis of spectroscopic methods and physicochemical properties as obtusifoline-2-O-ß-d-2, 6-di-O-acetylglucopyranoside (1), obtusifoline-2-O-ß-d-glucopyranoside (1a), obtusifoline-2-O-ß-d-3, 6-di-O-acetylglucopyranoside (2), and obtusifoline-2-O-ß-d-4, 6-di-O-acetylglucopyranoside (3).

Study of the Mechanism of Action of Guanxin Shutong Capsules in the Treatment of Coronary Heart Disease Based on Metabolomics.

Background: Guan-Xin-Shu-Tong capsule (GXSTC) is a traditional Chinese medicine (TCM) that has been used to treat coronary heart disease (CHD) for many years in China. However, the holistic mechanism of GXSTC against CHD is still unclear. Therefore, the purpose of this paper was to systematically explore the mechanism of action GXSTC in the treatment of CHD rats using a metabolomics strategy. Methods: A CHD model was induced by ligation of the left anterior descending coronary artery (LAD). In each group, echocardiography was performed; the contents of creatine kinase (CK), lactate dehydrogenase (LDH) and aspartate transaminase (AST) in serum were determined; and the myocardial infarct size was measured. The metabolites in plasma were analyzed by UHPLC-MS/MS-based untargeted metabolomics. Then, multivariate statistical analysis was performed to screen potential biomarkers associated with the GXSTC treatment in the LAD-induced rat CHD model. Finally, the MetaboAnalyst 4.0 platform was used for metabolic pathway enrichment analysis. Results: GXSTC was able to regulate the contents of CK, LDH and AST; restore impaired cardiac function; and significantly reduce the myocardial infarction area in model rats. Twenty-two biomarkers and nine metabolic pathways of GXSTC in the treatment of CHD were identified through UHPLC-MS/MS-based untargeted metabolomics analysis. Conclusion: GXSTC regulates metabolic disorders of endogenous components in LAD-induced CHD rats. The anti-CHD mechanism of GXSTC is mainly related to the regulation of amino acid, lipid and hormonal metabolism. This study provides an overall view of the mechanism underlying the action of GXSTC against CHD.

Melatonin protects against Nickel-induced neurotoxicity in vitro by reducing oxidative stress and maintaining mitochondrial function.

Nickel is a potential neurotoxic pollutant. Oxidative stress is supposed to be involved in the mechanism underlying nickel-induced neurotoxicity. Melatonin has efficient protective effects against various oxidative damages in nervous system. The purpose of this study was to investigate whether melatonin could efficiently protect against neurotoxicity induced by nickel. Here, we exposed primary cultured cortical neurons and mouse neuroblastoma cell lines (neuro2a) to different concentrations of nickel chloride (NiCl(2)) (0.125, 0.25, 0.5, and 1 mm) for 12 hr or 0.5 mm NiCl(2) for various periods (0, 3, 6, 12, and 24 hr). We found that nickel significantly increased reactive oxygen species production and caused the loss of cell viability both in cortical neurons and neuro2a cells. In addition, nickel exposure obviously inhibited the mitochondrial function, disrupted the mitochondrial membrane potential (DeltaPsim), reduced ATP production, and decreased mitochondrial DNA (mtDNA) content. However, each of these oxidative damages was efficiently attenuated by melatonin pretreatment. These protective effects of melatonin may be attributable to its roles in reducing oxidative stress and improving mitochondrial function in nickel-treated nerve cells. Our results suggested that melatonin may have great pharmacological potential in protecting against the adverse effects of nickel in the nervous system.

Immunosuppressive sesquiterpenes from Buddleja daviddi.

Six new sesquiterpenes, 2,6(12),10-humulatrien-7ß-ol-1-one (1), 2 α-acetoxy-5α-methoxy-enantio-caryophylla-8(15)-en-3-one (2), 2α-acetoxy-5α-hydroxy-enantio-caryophylla-8(15)-en-3-one (3), 2α-acetoxy-4ß,5α-hydroxy-enantio-caryophylla-8(15)-en-3-one ( 4), 2α-acetoxy-4ß,5ß-hydroxy-enantio-caryophylla-8(15)-en-3-one (5), 2ß-acetoxy-4-caryophyllen-8ß-ol-3-one (6), and nineteen known compounds were isolated from the ethanol extract of Buddleja daviddi. The structures were elucidated by spectroscopic methods. Compounds 8-11, 14, 16, 17, and 20 showed significant immunosuppressive activities, and 8-11 and 14 were cytotoxic on HeLa and L929 cell lines.

[Measurement of the cross section in Li(2P)+H2-->LiH+H reaction].

At a Li density of approximately 10(13) cm(-3), the lithium vapor was irradiated in a five-arm stainless steel heat pipe oven containing Li and H2 with pulses of radiation from a N2-laser-pumped dye laser, populating Li(2P) state by the Li(2S-->2P) resonance transition at 670.8 nm. Typical operating pressure of H2 was 60-300 Pa. The cross section for Li(2P)+H2-->LiH+H reaction was measured using method of atomic fluorescence. The decay signal of the time-resolved fluorescence from the 2P-->2S transition was monitored. The decay curve of the Li(2P) can be treated as a single exponential function. The effective lifetimes of the 2P state was obtained. According to the Stern-Volmer equation, a plot of reciprocal of effective lifetimes of the 2P state quenched by H2 against its densities yielded a slope that indicated the total cross section for deactivation and an intercept (at which the H2 pressure is zero) that provided the information about the radiative lifetime of the state. The total quenching (reactive+nonreactive) cross section for deactivation of the 2P state by means of collisions with H2 is (25.1 +/- 4.0) x 10(-16) cm2. The reactive cross section could be obtained using results of the recording of the fluorescence signals with rapid rise in transient regime (<10 ns) Li(2P-->2S) at the different H2 densities. The authors fitted a two-state rate equation model to obtain the cross section sigma (Li(2P)+H2-->LiH+H) = (0.2 +/- 0.1) x 10(-16) cm2. The authors' results imply that reactive collisions occur on average 1/125 as often as quenching collisions. The cross section for reaction is small but not negligible.

Structure-Dependent Antibacterial Activity of Amino Acid-Based Supramolecular Hydrogels.

Bacterial infections are currently a major concern to human health. Amino acid-based supramolecular polymer hydrogels, which boast intrinsic antibacterial activity, are an important solution due to their good biocompatibility, cost effectiveness, and tunable structural properties. Herein, we reported three types of transparent supramolecular hydrogel with intrinsic antibacterial activity from self-assembly of commercially available Fmoc-tryptophan (Fmoc-W), Fmoc-methionine (Fmoc-M), and Fmoc-tyrosine (Fmoc-Y). The resulting hydrogels selectively inhibited the growth of Gram-positive bacteria. Moreover, the order of antibacterial activity was Fmoc-W hydrogel > Fmoc-M hydrogel > Fmoc-Y hydrogel. The critical aggregation concentration (CAC) values were found at concentrations of approximately 0.0293, 0.1172, and 0.4688 mM for Fmoc-W, Fmoc-M, and Fmoc-Y, respectively. Transmission electron microscope (TEM) images revealed rigid and aligned nanofibers for Fmoc-W hydrogel, while flexible nanofibers for Fmoc-M hydrogel and Fmoc-Y hydrogel. The results indicated that stronger aggregation capability of the gelator and the synergistic nanostructural morphology with more rigid and aligned nanofibers can lead to higher antibacterial activity of its corresponding hydrogel. In addition, the molecular arrangements of Fmoc-amino acids in the hydrogels may also contribute to their antibacterial activity. These results can guide the rational design, fabrication, and future application of other self-assembled amino acid-based hydrogels with excellent antibacterial activity.

Development and antibacterial activities of bacterial cellulose/graphene oxide-CuO nanocomposite films.

The absence of antibacterial activity of bacterial cellulose (BC) restricts its applications in the biomedical field. To introduce antimicrobial properties into BC, we studied the synthesis, structure, and antimicrobial properties of a novel nanocomposite film comprising BC, graphene oxide (GO), and copper-oxide (CuO) nanosheets. The nanocomposite film was synthesized by incorporating GO-CuO nanohybrids into BC matrix through homogenized blending. The CuO nanosheets, with a length range of 50 nm-200 nm and width range of 20 nm-50 nm, which were uniformly grown on the GO along with even distribution of GO-CuO nanohybrids on the surface of the cellulose fibers. The nanocomposites displayed better antibacterial activity against gram-positive than gram-negative bacteria. BC/GO-CuO nanocomposites showed higher antibacterial activity than BC/CuO. We also elucidated the mechanism of antibacterial activity of the nanocomposites. Further, the nanocomposites exhibited biocompatibility towards mice fibroblast cells. The nanocomposites might serve as an excellent source for development of antibacterial materials.

Network pharmacology-based prediction of the active ingredients and mechanism of Shen Gui capsule for application to coronary heart disease.

BACKGROUND: Shen Gui capsule (SGC) is a new national drug in China that is widely used in clinical practice and has significant therapeutic effects on coronary heart disease (CHD). However, its active ingredients and mechanism of action for treating coronary heart disease remain unknown. Therefore, the purpose of this paper is to systematically explore the mechanism and efficacy of SGC in the "multicomponent-multitarget- multipathway" treatment for CHD using network pharmacology technology. METHODS: The potential active ingredients of SGC were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and screened by pharmacokinetic parameters. Their possible targets were predicted using the TCMSP and DrugBank database. The CHD-related targets were identified from Comparative Toxicogenomics Database (CTD), UniProt, and PharmGKB database. The compound-target-disease network was constructed using Cytoscape for visualization. Additionally, the protein functional annotation and identification of signaling pathways of potential targets were performed by Gene Ontology (GO) and KEGG enrichment analysis using the Metascape platform. RESULTS: The 61 active ingredients of SGC were found to regulate neuroactive ligand-receptor interaction, fluid shear stress and atherosclerosis, estrogen signaling pathway and other pathways through 62 targets. SGC is involved in regulating the circulatory system, nervous system and immune system and other aspects of the body, and thus plays a significant role in the treatment of CHD and its complications, showing the mechanism of SGC's "multicomponent, multitarget, and multipathway" prevention and treatment of CHD. In addition, three predictive components were first found to have potential biological activity by this method. CONCLUSION: The studies we have performed successfully predict the effective components and potential targets of SGC in the prevention and treatment of CHD, which helped to systematically clarify its mechanism of action and provided a direction for future research on the modern mechanism of SGC in the treatment of CHD.

Differential effects of nectar robbing by the same bumble-bee species on three sympatric Corydalis species with varied mating systems.

BACKGROUND AND AIMS: Most research on the widespread phenomenon of nectar robbing has focused on the effect of the nectar robbers' behaviour on host-plant fitness. However, attention also needs be paid to the characteristics of host plants, which can potentially influence the consequences of nectar robbing as well. A system of three sympatric Corydalis species sharing the same nectar-robbing bumble-bee was therefore studied over 3 years in order to investigate the effect of nectar robbing on host reproductive fitness. METHODS: Three perennial species of Corydalis were studied in the Shennongjia Mountain area, central China. Observations were conducted on visitor behaviour and visitation frequencies of nectar-robbers and legitimate pollinators. KEY RESULTS: The results indicated that the effect of nectar robbing by Bombus pyrosoma varied among species, and the three species had different mating systems. Seed set was thus influenced differentially: there was no effect on seed set of the predominantly selfing C. tomentella; for the facultative outcrossing C. incisa, nectar robbing by B. pyrosoma had a positive effect; and nectar robbing had a significant negative effect on the seed set of outcrossing C. ternatifolia. CONCLUSIONS: A hypothesis is proposed that the type of host-plant mating system could influence the consequences of nectar robbing on host reproductive fitness.

Six new cycloartane triterpene glycosides from Actaea asiatica.

Six new cycloartane triterpene glycosides, (3',12beta)-O-diacetyl-cimigenol-3-O-beta-D-xylopyranoside (1), (4',25)-O-diacetyl-cimigenol-3-O-beta-D-xylopyranoside (2), 2'-O-acetyl-25-O-methyl-cimigenol-3-O-beta-D-xylopyranoside (3), 2'-O-acetyl-25-O-ethyl-cimigenol-3-O-beta-D-xylopyranoside (4), 3'-O-acetyl-cimicifugoside (5), and 4'-O-acetyl-23-epi-26-deoxycimifugoside (6), were isolated from the rhizomes of Actaea asiatica. Their structures were elucidated on the basis of chemical methods and spectroscopic analysis. Compounds 1, 2, 4-6 exhibited positive cytotoxic activities.

[Measurement of fine-structure branching ratios for Rb-He optical collisions].

Experimental ratios of branching in the fine-structure levels of the Rb5P multiplet, as a consequence of an optical collision with He, are reported. The process studied is Rb(5S1/2 )+ He + hrv --> Rb(5P(J)) +He, where the pulsed laser frequency v is tuned in the wings of the Rb resonance transitions. The authors defined the detuning delta to be v-v (D2 )(delta > 0) for laser frequency v highter than that of RbD2 transition and to be v-v (D1)(delta < 0) for v lower than the RbD1 transition. As RbHe molecular states are correlated to the two 5 2P(J) states, there is some likelihood that the molecule will dissociate into 5 2P1/2 or 5P3/2 state. The dissociation results in a nonuniform distribution of atomic Rb5P(J) states. The branching ratios are defined as n1/n2, where n1 and n2 are densities of the 5P1/2 and 5P3/2 states dissociated. To determine experimentally the relative cross section for scattering into the two fine-structure states, the relative time-intergrated intensities of the resulting Rb emission lines, I(5P3/2 --> 5P1/2 )[I(D2)] and I(5P1/2 --> 5P3/2) ) [I(D1)], were measured. The ratios are determined by detunings from about 200 cm(-1) in the blue wing to -180 cm(-1) in the red wing of the Rb5P multiplet. A rate equation analysis of the pressure dependence was yielded. The branching ratios and cross sections for collisional 5P1/2 --> 5P3/2 transition were obtained from the slope and intercept. The blue-wing branching ratios show a detuning-dependent approach to limit of 0. 2. The branching was found to be very large (-40) in the red wing, irrespective of the detuning. Fine structure changing cross section (1.1 +/- 0.3) x 10(-17) cm2 was measured from wing excitation, and the result is consistent with the cross section obtained from resonant excitation of the Rb5P(J) state. The measurements show a strong sensitivity to interatomic potentials and to nonadiabatic effects in dissociation dynamics.

[Reactive and nonreactive energy transfer in Cs(6D(J))+ (H2, He) collisions].

Cs vapor, mixed with a gas was irradiated in a glass fluorescence cell with pulses of 886nm radiation from a YAG-laser-pumped OPO laser, populating 6D3/2 state by two-photon absorption. Cross sections for 6D3/2 --> 6D5/2 transition induced by collisions with various H(e) atoms and H2 molecules were determined using methods of atomic fluorescence. The resulting fluorescence included a direct component emitted in the decay of the optically excited state and a sensitized component arising from the collisionally populated state. At the different densities, we have measured the relative time-integrated intensities of the components and fitted a three-state rate equation model to obtain the cross sections for 6D3/2 --> 6D5/2 transfer: sigma = (55 +/- 13) x 10(-16) and (16 +/- 4) x 10(-16) cm2 for H2 and H(e), respectively. The cross sections for the effective quenching of the 6D5/2 state were also determined. The total transfer rate coefficients from the 6D5/2 state for H(e) is small [1.2 x 10(-10) cm3 x s(-1)]. The total quenching rate coefficient of the 6D5/2 state is larger for H2 [6.7 x 10(-10) cm3 z s(-1)]. For H2 case, the quenching rate coefficient corresponds to reaction and nonreactive energy transfer. Evidence suggests that the nonreactive energy transfer rate coefficient is [6.3 x 10(-10) cm3 x s(-1)]. Hence the authors estimated the cross section (2.0 +/- 0.8) x 10(-16) cm2 for reactive process Cs(6D5/2) + H2 --> CsH + H. Using the dependence on the pressure of H2 (or H(e)) of the integrated fluorescence monitored at the 6D5/2 --> 6P3/2 transition the cross section (4.0 +/- 1.6) x 10(-16) cm2 for Cs (6D3/2) + H2 --> CsH + H was obtained. Thus, the relative reactivity with H2 follows an order of Cs (6D3/2) > Cs (6D5/2).

Expression of tumor necrosis factor receptor 2 in human non-small cell lung cancer and its role as a potential prognostic biomarker.

BACKGROUND: Tumor necrosis factor receptor 2 (TNFR2) promotes tumor cell proliferation, activates immunosuppressive cells, and supports immune escape. However, its role in non-small cell lung cancer (NSCLC) has not been reported. METHODS: Quantitative real-time PCR and Western blotting were used to evaluate TNFR2 in three NSCLC cell lines (A549, H1299, H1975) and normal lung epithelial cells (BEAS-2B). TNFR2 was evaluated in 71 tumor tissues and 25 adjacent normal lung tissues by immunohistochemistry and analyzed with respect to clinical parameters. RESULTS: The messenger RNA and protein levels of TNFR2 were significantly higher in A549, H1299, and H1975 cells than in BEAS-2B cells (P < 0.05) and differed significantly between NSCLC tissues and adjacent normal lung tissues by immunohistochemistry (P < 0.0001). TNFR2 is a independent prognostic factor in NSCLC. There have significantly differences in overall survival (OS) (P = 0.006) and disease-free survival (DFS) (P = 0.000) of NSCLC patients between TNFR2 low expression groups and TNFR2 high expression group. CONCLUSION: TNFR2 is expressed in human NSCLC tissues and cell lines and is related to poor prognosis. TNFR2 may represent a new auxiliary index for patients with NSCLC.

[Study on anti-diabetes active fraction and constituents from Potentilla chinesis].

OBJECTIVE: To study the active fraction and constituents from Potentilla chinesis. METHOD: Tested fractions were obtained by different solvent-partition from 95% ethanol-extracts of P. chinesis, and tested compound was isolated by repeated chromatography. Anti-diabetes experiment was taken by using alloxan-induced diabetic mice. RESULT: The fraction F and the tested compound revealed obvious difference comparing with the control group (P <0.01). CONCLUSION: Fraction F and potentilla flavone revealed the significant hypoglycemic effect in alloxan-induced diabetic mice.

[Studies on chemical constituents from rhizome of Anemone flaccida].

OBJECTIVE: To study the chemical constituents from Anemone flaccida. METHOD: Chemical constituents were isolated by repeated column chromatography (silica gel, Toyopearl HW-40C and preparative HPLC). The structures were elucidated on the basis of spectral data analysis. RESULT: Twelve triterpenes were isolated and their structures were identified as follow: oleanolic acid (1), oleanolic acid 3-O-beta-D-glccopyranosyl-(1-->2)-beta-D-xylopyranoside (2), eleutheroside K (3), oleanolic acid 3-O-alpha-L-rhamnopyranosyl-(1-->2)-beta-D-xylopyranoside (4), oleanolic acid 3-O-beta-D-glccopyranosyl-(1-->2)-alpha-L-arabinofurnoside (5), oleanolic acid 3-O-beta-D-glccuronopyranose (6), oleanolic acid 3-O-beta-D-glccuronopyranose methyl ester (7), oleanolic acid 28-O-alpha-L-rhamnopyranosyl(1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranosyl (8), oleanolic acid 3-O-beta-D-glccuronopyranose 28-O-alpha-L-rhamnopyranosyl (1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranoside (9), oleanolic acid 3-O-beta-D-glccopyranosyl methyl ester 28-O-alpha-L-rhamnopyranosyl (1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranoside (10), oleanolic acid 3-O-beta-D-glccopyranosyl-(1-->2)-beta-D-xylopyranosyl-28-O-alpha-L-rhamnopyranosyl (1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranoside (11), oleanolic acid 3-O-alpha-L-rh-amnopyranosyl-(1-->2)-alpha-L-arabinopyrnosyl-28-O-alpha-L-rhamnopyranosyl (1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranoside (12). CONCLUSION: compounds 5-8, 10, 12 were isolated from this plant for the first time. Compounds 2, 5 and 11 showed positive anti-tumor activities.