Serum pro-BDNF/BDNF as a treatment biomarker for response to docosahexaenoic acid in traumatized people vulnerable to developing psychological distress: a randomized controlled trial.

Our open-label pilot study showed that supplementation with docosahexaenoic acid (DHA) increased serum brain-derived neurotrophic factor (BDNF) levels and that there might be an association between changes in serum BDNF levels and reduced psychological distress. Animal research has indicated that a DHA-enriched diet increases BDNF in the brain. In this randomized double-blind controlled trial of severely injured patients vulnerable to posttraumatic stress disorder (PTSD) and depression, we examined whether DHA increases serum BDNF levels and whether changes in BDNF levels are associated with subsequent symptoms of PTSD and depression. Patients received 1470 mg per day of DHA plus 147 mg per day of eicosapentaenoic acid (EPA; n = 53) or placebo (n = 57) for 12 weeks. Serum levels of mature BDNF and precursor pro-BDNF at baseline and 12-week follow-up were measured using enzyme-linked immunosorbent assay kits. At 12 weeks, we used the Clinician-Administered PTSD Scale to assess PTSD symptoms and depressive symptoms by the Montgomery-Åsberg Depression Rating Scale. We found a significant increase in serum BDNF levels during the trial in the DHA and placebo groups with no interaction between time and group. Changes in BDNF levels were not associated with PTSD severity but negatively associated with depression severity (Spearman's ρ = -0.257, P = 0.012). Changes in pro-BDNF were also negatively associated with depression severity (Spearman's ρ = -0.253, P = 0.013). We found no specific effects of DHA on increased serum levels of BDNF and pro-BDNF; however, evidence in this study suggests that increased BDNF and pro-BDNF have a protective effect by minimizing depression severity.

Super-high-dose islet transplantation is associated with high SUITO index and prolonged insulin independence: a case report.

INTRODUCTION: One of the current issues of clinical islet transplantation is the difficulty to achieve a prolonged insulin-free status. Functional islet mass gradually decreased after transplantation. We developed the SUITO index, which reflects engrafted islet mass. The SUITO (Secretory Unit of Islet Transplant Objects) index more than 26.0 is associated with an insulin-free status. In this study, we have experienced that super-high-dose islet transplantation maintained insulin-free status and a high SUITO index for a prolonged period. MATERIALS AND METHODS: Two islet isolations were performed in February 2007 and January 2008. Ductal injections were performed at the procurement site using the ET-Kyoto solution and pancreata preserved by a two-layer method. Islets were isolated using the modified Ricordi method. Both isolated islets were transplanted into a type 1 diabetic patient. Efficacy of islet transplantation was assessed by the amount of insulin requirements and SUITO index. RESULTS: Islet yields were 514,467 islet equivalents (IE) and 872,174 IE, with purities of 49% and 85% for the first and second islet transplantations, respectively. The patient received a total of 24,327 IE/kg body weight. The immunosuppression was based on the Edmonton protocol. After the second islet transplantation, the average SUITO index for the following 1 month was 48.5, and the patient became insulin-free. At postoperative day 1006, the SUITO index was 44.6 and the patient maintained an insulin-free status with excellent glycemic control. CONCLUSION: Super-high-dose islet transplantation was associated with an high SUITO index and prolonged insulin independence.

Anti-obesity and anti-diabetic effects of brain-derived neurotrophic factor in rodent models of leptin resistance.

OBJECTIVE: Obesity in rodents and humans is mostly associated with elevated plasma leptin concentrations, suggesting a new pathological concept of 'leptin resistance'. We have demonstrated that brain-derived neurotrophic factor (BDNF) can improve obesity and diabetes of C57BL/KsJ db/db (db/db) mice. In this study, we investigated whether or not BDNF is effective in two different models of leptin resistance, an acquired model and a genetic model. DESIGN: C57BL/6J mice rendered obese by consumption of a high-fat diet (diet-induced obesity (DIO) mice) were used as an acquired model and lethal yellow agouti mice (KKA(y) mice) as a genetic model of leptin resistance. Food intake and glucose metabolism were studied after acute or repetitive administration of BDNF. RESULTS: Intraperitoneal administration of BDNF (10 mg/kg, twice/day) significantly reduced cumulative food intake of DIO and KKA(y) mice, whereas they were unresponsive to leptin administration. Repetitive subcutaneous administration of BDNF (10 mg/kg daily for 6 days) reduced food intake and improved impaired glucose tolerance in DIO mice. Pair feeding of vehicle-treated DIO mice with the same amount of chow consumed by the BDNF-treated group did not improve the impaired glucose homeostasis, indicating that the antidiabetic effect is not due to decreased food intake. We also observed that BDNF is effective in improving obesity and diabetes of KKA(y) mice. CONCLUSION: This study demonstrated antiobesity and antidiabetic effects of BDNF in two different models of leptin resistance, thereby suggesting the therapeutic potential of BDNF in the treatment of leptin-resistant obesity and diabetes.

Benzalacetone synthase. A novel polyketide synthase that plays a crucial role in the biosynthesis of phenylbutanones in Rheum palmatum.

Benzalacetone synthase (BSA) is a novel plant-specific polyketide synthase that catalyzes a one step decarboxylative condensation of 4-coumaroyl-CoA with malonyl-CoA to produce the C6-C4 skeleton of phenylbutanoids in higher plants. A cDNA encoding BAS was for the first time cloned and sequenced from rhubarb (Rheum palmatum), a medicinal plant rich in phenylbutanoids including pharmaceutically important phenylbutanone glucoside, lindleyin. The cDNA encoded a 42-kDa protein that shares 60-75% amino-acid sequence identity with other members of the CHS-superfamily enzymes. Interestingly, R. palmatum BAS lacks the active-site Phe215 residue (numbering in CHS) which has been proposed to help orient substrates and intermediates during the sequential condensation of 4-coumaroyl-CoA with malonyl-CoA in CHS. On the other hand, the catalytic cysteine-histidine dyad (Cys164-His303) in CHS is well conserved in BAS. A recombinant enzyme expressed in Escherichia coli efficiently afforded benzalacetone as a single product from 4-coumaroyl-CoA and malonyl-CoA. Further, in contrast with CHS that showed broad substrate specificity toward aliphatic CoA esters, BAS did not accept hexanoyl-CoA, isobutyryl-CoA, isovaleryl-CoA, and acetyl-CoA as a substrate. Finally, besides the phenylbutanones in rhubarb, BAS has been proposed to play a crucial role for the construction of the C6-C4 moiety of a variety of natural products such as medicinally important gingerols in ginger plant.

Hypoleptinemia, but not hypoinsulinemia, induces hyperphagia in streptozotocin-induced diabetic rats.

To assess the dominance between hypoinsulinemia and hypoleptinemia as factors in the development of hyperphagia in streptozotocin (STZ)-induced diabetes mellitus (STZ-DM) rodents with respect to hormone-neuropeptide interactions, changes in gene expression of agouti gene-related protein (AGRP) in the arcuate nucleus of the hypothalamus were investigated using STZ-DM rats, fasting Zucker fa/fa rats and STZ-DM agouti (STZ-DM A(y)/a) mice. AGRP mRNA and neuropeptide Y mRNA were both significantly up-regulated in STZ-DM rats, which are associated with body weight loss, hyperglycemia, hypoinsulinemia and hypoleptinemia. We proceeded to analyze whether insulin or leptin played the greater role in the regulation of AGRP using Zucker fa/fa rats. The AGRP mRNA did not differ significantly between fasted fa/fa rats, which have both leptin-insensitivity and hypoinsulinemia, and fed Zuckers, which have leptin-insensitivity and hyperinsulinemia. We further found that up-regulation of AGRP expression was normalized by infusion of leptin into the third cerebroventricle (i3vt), but not by i3vt infusion of insulin, although up-regulation of AGRP was partially corrected by systemic insulin infusion. The latter finding supports hypoleptinemia as a key-modulator of STZ-DM-induced hyperphagia because systemic insulin infusion, at least partially, restored hypoleptinemia through its acceleration of fat deposition, as demonstrated by the partial recovery of lost body weight. After STZ-DM induction, A(y)/a mice whose melanocortin-4 receptor (MC4-R) was blocked by ectopic expression of agouti protein additionally accelerated hyperphagia and up-regulated AGRP mRNA, implying that the mechanism is triggered by a leptin deficit rather than by the main action of the message through MC4-R. Hypoleptinemia, but not hypoinsulinemia per se, thus develops hyperphagia in STZ-DM rodents. These results are very much in line with evidence that hypothalamic neuropeptides are potently regulated by leptin as downstream targets of its actions.

Green tea polyphenols as potent enhancers of glucocorticoid-induced mouse mammary tumor virus gene expression.

The effect of natural and synthetic galloyl esters on glucocorticoid-induced gene expression was evaluated by using rat fibroblast 3Y1 cells stably transfected with a luciferase reporter gene under the transcriptional regulation of the mouse mammary tumor virus promoter. The glucocorticoid-induced gene transcription was strongly suppressed by synthetic alkyl esters; n-dodecyl gallate showed the most potent inhibition (66% inhibition at 10 microM), which was far more potent than that of crude tannic acid. n-Octyl and n-cetyl gallate also showed good inhibition, while gallic acid itself was not so active, suggesting that the presence of hydrophobic side chain is important for the suppressive effect. On the other hand, surprisingly, green tea gallocatechins, (-)-epigallocatechin-3-O-gallate and theasinensin A, potently enhanced the promoter activity (182 and 247% activity at 1 microM, respectively). The regulation of the level of the glucocorticoid-induced gene expression by the antioxidative gallates is of great interest from a therapeutic point of view.

Does physician specialty affect the survival of elderly patients with myocardial infarction?

OBJECTIVE: To determine the effect of treatment by a cardiologist on mortality of elderly patients with acute myocardial infarction (AMI, heart attack), accounting for both measured confounding using risk-adjustment techniques and residual unmeasured confounding with instrumental variables (IV) methods. DATA SOURCES/STUDY SETTING: Medical chart data and longitudinal administrative hospital records and death records were obtained for 161,558 patients aged > or =65 admitted to a nonfederal acute care hospital with AMI from April 1994 to July 1995. Our principal measure of significant cardiologist treatment was whether a patient was admitted by a cardiologist. We use supplemental data to explore whether our analysis would differ substantially using alternative definitions of significant cardiologist treatment. STUDY DESIGN: This retrospective cohort study compared results using least squares (LS) multivariate regression with results from IV methods that accounted for additional unmeasured patient characteristics. Primary outcomes were 30-day and one-year mortality, and secondary outcomes included treatment with medications and revascularization procedures. DATA COLLECTION/EXTRACTION METHODS: Medical charts for the initial hospital stay of each AMI patient underwent a comprehensive abstraction, including dates of hospitalization, admitting physician, demographic characteristics, comorbid conditions, severity of clinical presentation, electrocardiographic and other diagnostic test results, contraindications to therapy, and treatments before and after AMI. PRINCIPAL FINDINGS: Patients admitted by cardiologists had fewer comorbid conditions and less severe AMIs. These patients had a 10 percent (95 percent CI: 9.5-10.8 percent) lower absolute mortality rate at one year. After multivariate adjustment with LS regression, the adjusted mortality difference was 2 percent (95 percent CI: 1.4-2.6 percent). Using IV methods to provide additional adjustment for unmeasured differences in risk, we found an even smaller, statistically insignificant association between physician specialty and one-year mortality, relative risk (RR) 0.96 (0.88-1.04). Patients admitted by a cardiologist were also significantly more likely to have a cardiologist consultation within the first day of admission and during the initial hospital stay, and also had a significantly larger share of their physician bills for inpatient treatment from cardiologists. IV analysis of treatments showed that patients treated by cardiologists were more likely to undergo revascularization procedures and to receive thrombolytic therapy, aspirin, and calcium channel-blockers, but less likely to receive beta-blockers. CONCLUSIONS: In a large population of elderly patients with AMI, we found significant treatment differences but no significant incremental mortality benefit associated with treatment by cardiologists.

Oligosaccharide esters from the roots of Polygala arillata.

Two new sucrose esters, arillatoses A (1) and B (2), and four new trisaccharide esters, arillatoses C-F (3-6), were isolated from the roots of Polygala arillata, together with four known sucrose esters, glomeratose E (7) and sibiricoses A(1) (8), A(5) (9), and A(6) (10). The structures of the new compounds were elucidated on the basis of chemical and spectroscopic evidence.

Tetrasaccharide multi-esters and xanthone glycosides from the roots of Polygala wattersii.

Ten new tetrasaccharide multi-esters, watteroses A-J (1-10), and two new xanthone glycosides, wattersiixanthones A (11) and B (12), were isolated from the roots of Polygala wattersii, together with 11 known compounds (10 oligosaccharide multi-esters and a xanthone glycoside). The structures of new compounds were elucidated on the basis of chemical and spectroscopic evidence.

Green tea polyphenols: novel and potent inhibitors of squalene epoxidase.

The green tea gallocatechins, (-)-epigallocatechin-3-O-gallate (EGCG) (IC(50) = 0.69 microM), (-)-gallocatechin-3-O-gallate (GCG) (IC(50) = 0.67 microM), (-)-epicatechin-3-O-gallate (ECG) (IC(50) = 1.3 microM), and theasinensin A (IC(50) = 0.13 microM), were found to be potent and selective inhibitors of rat squalene epoxidase (SE), a rate-limiting enzyme of cholesterol biogenesis. On the other hand, flavan-3-ols without galloyl group at C-3 did not show significant enzyme inhibition. It was demonstrated for the first time that the cholesterol lowering effect of green tea may be attributed to their potent SE inhibition activities. Inhibition kinetics revealed that EGCG inhibited SE in noncompetitive (K(I) = 0.74 microM), and non-time-dependent manner. The potent enzyme inhibition would be caused by specific binding to the enzyme, and by scavenging reactive oxygen species required for the monooxygenase reaction.

Galloyl esters from rhubarb are potent inhibitors of squalene epoxidase, a key enzyme in cholesterol biosynthesis.

Galloyl glucoses and galloyl proanthocyanidins obtained from rhubarb (Rhei Rhizoma, Rheum palmatum L., Polygonaceae); e.g. 1,2,6-tri-O-galloyl-beta-D-glucose (IC50 = 0.63 microM), 1,6-di-O-galloyl-2-O-cinnamoyl-beta-D-glucose (IC50 = 0.58 microM), procyanidin B-2 3,3'-di-O-gallate (IC50 = 0.54 microM), and procyanidin B-5 3,3'-di-O-gallate (IC50 = 0.55 microM), were found to be potent inhibitors of rat squalene epoxidase (SE). The inhibition at submicromolar level was far more potent than that of chemically synthesized substrate analogs. It was demonstrated for the first time that the cholesterol-lowering effect of rhubarb may be attributed to the potent inhibition activities of SE, a rate-limiting enzyme of cholesterol biogenesis.

Role of rapid focal activation in the maintenance of atrial fibrillation originating from the pulmonary veins.

Most episodes of focal atrial fibrillation (AF) can be initiated by premature beats originating from the pulmonary veins (PV). However, the role of rapid focal activation in the maintenance of AF is unclear. Thirty-two patients with focal AF who underwent focal ablation of triggering ectopic beats were studied. Bipolar electrograms from all four PVs were recorded simultaneously. The cycle length (CL) of RFA at sites that triggered AF was measured at AF onset, after 5 minutes of sustained AF, and just before the spontaneous termination of 32 episodes of nonsustained AF. Fifteen episodes of sustained AF (> 10 minutes) and 17 episodes of nonsustained AF (5-120 seconds, mean 56 +/- 59 seconds) were analyzed. In sustained AF, the mean CL of RFA in the PV from which it originated was not significantly different than in the other PVs, and RFA was continuously observed. In nonsustained AF, the mean CL of RFA in a PV from which it originated was significantly shorter than in other PVs and, when RFA disappeared, AF terminated. RFA in 1 PV induced RFA in another PV. In conclusion, widespread conduction of RFA from a PV at its source to the other sites may be necessary for the sustenance of AF. A PV interaction, a RFA triggering another, may be involved in the maintenance of AF. RFA arising from PVs is important not only as a trigger of onset, but also in the maintenance of AF.

Plasma fatty acids concentrations in postoperative patients with biliary atresia.

The concentrations of plasma fatty acids in postoperative patients with biliary atresia (BA) were measured to clarify whether they had essential fatty acid deficiency. Thirty-eight fasting blood samples from 14 postoperative patients with BA were studied. All of them had the hepatic portoenterostomy without any stoma. Samples were divided into three groups on the basis of liver function. The concentrations of fatty acids in the plasma fat were measured quantitatively. Non-essential fatty acids levels were increased and omega-3 fatty acids levels were decreased with the progress of deterioration of hepatic function. Regarding omega-6 fatty acids, C18:2 and 20:4 did not show any significant difference between the three groups and the control, and only C20:3 increased with the deterioration of liver dysfunction. The ratio of C20:3 (omega-6) to C20:4 (omega-6) was increased significantly with the progress of liver dysfunction. The activity of delta-5 desaturase was suspected to be suppressed in BA patients with poor liver function. The BA patients with poor bile flow did not show any decrease of omega-6 fatty acids in the plasma, but were at risk of developing omega-3 fatty acid deficiency.

Triterpenoid saponins from Ilex kudincha.

Ten new triterpene saponins, ilekudinosides A-J (2, 6-8, 10, 13-17), together with seven known triterpene saponins, ilexoside XLVIII (1); cynarasaponin C (5); latifolosides A (9), C (3), G (12), and H (4); and kudinoside G (11), were isolated from an aqueous extract of the leaves of Ilex kudincha. They possessed oleanane- and ursane-type triterpenoids as the aglycons. The structures were elucidated by 1D and 2D NMR experiments, including ROE difference, HOHAHA difference, 1H-1H COSY, and 1H-13C COSY (HMQC, HMBC) methods and sugar analysis. Compounds 1 and 5 exhibited acyl CoA cholesteryl acyl transferase (ACAT) inhibitory activity.

Sucrose esters and xanthone C-glycosides from the roots of Polygala sibirica.

Six new sucrose esters, sibiricoses A(1)-A(6) (1-6), two new xanthone C-glycosides, sibiricaxanthones A (7) and B (8), and a new acetophenone glycoside, sibiricaphenone (9), were isolated from the roots of Polygala sibirica together with six known glycosides. The structures of new compounds were elucidated on the basis of chemical and spectroscopic evidence. The structure of the known xanthone glycoside, polygalaxanthone III (10), was revised.

Activity-guided isolation of triterpenoid acyl CoA cholesteryl acyl transferase (ACAT) inhibitors from Ilex kudincha.

Activity-guided fractionation of a methanol extract of the leaves of Ilex kudincha led to the isolation of seven acyl CoA cholesteryl acyl transferase (ACAT) inhibitory triterpenes. Four of them were identified by spectroscopic methods as ulmoidol (4), 23-hydroxyursolic acid (5), 27-trans-p-coumaroyloxyursolic acid (6), and 27-cis-p-coumaroyloxyursolic acid (7), and three were new compounds named ilekudinols A-C (1-3). The structures of these new triterpenoids were elucidated as 2alpha, 3beta-dihydroxy-24-nor-urs-4(23),11-dien-28,13beta- olide (1), 2alpha, 3beta-dihydroxy-24-nor-urs-4(23),12-dien-28-oic acid (2), and 3beta, 24,28-trihydroxylupane (3). Compounds 1-7 showed potent inhibitory activity in the ACAT assay.

Gene for a protein capable of enhancing lateral root formation.

Analysis of genes preferentially expressed in hairy roots caused by infection with Agrobacterium rhizogenes has provided insights into the regulation of lateral root formation. A hairy root preferential cDNA, HR7, has been cloned from hairy roots of Hyoscyamus niger. HR7 encodes a novel protein partially homologous to a metallocarboxypeptidase inhibitor and is expressed exclusively in the primordium and base of lateral roots in hairy roots. Overexpression of HR7 in transgenic roots of H. niger dramatically enhances the frequency of lateral root formation. The results of this study indicate that expression of HR7 plays a critical role in initiating lateral root formation.

Metastasis of hepatocellular carcinoma to the right colon manifested by gastrointestinal bleeding.

An 82-year-old black woman with a history of hepatocellular carcinoma presented with gastrointestinal bleeding. Barium enema and fibrocolonoscopy revealed a 4-cm polypoid mass at the level of the ascending colon with evidence of active bleeding. Biopsies of the lesion proved it to be metastatic hepatocellular carcinoma. Exploratory laparotomy revealed no further dissemination of the tumor, and the patient underwent an ileocolectomy. The serosal side of the colonic lesion was free from tumor, and there was no peritoneal implantation, direct extension, or lymph node involvement. This case represents an extremely rare presentation of metastatic hepatocellular carcinoma.

Oligosaccharide polyesters from roots of Polygala glomerata.

Seven new sucrose and oligosaccharide esters, glomeratoses A-G, together with four known compounds, 3-O-[(E)-3,4,5-trimethoxycinnamoyl]-beta-D-fructofuranosyl-(2-->1) - (6-O-benzoyl)-alpha-D-glucopyranoside, 3-O-(E)-sinapoyl-beta-D-fructofuranosyl-(2-->1)-[6-O-(E)-sinapo yl]-alpha-D- glucopyranoside, tenuifoliside C and reiniose G were isolated from the roots of Polygala glomerata. Glomeratoses A-G were elucidated as 3-O-[(E)-3,4,5-trimethoxycinnamoyl]-beta-D-fructofuranosyl-(2-->1) -alpha-D- glucopyranoside, 3-O-(E)-sinapoyl-beta-D-fructofuranosyl-(2-->1)-[6-O-(E)-p- coumaroyl]-alpha-D-glucopyranoside, 3-O-[(E)-3,4,5-trimethoxycinnamoyl]-beta-D-fructofuranosyl-(2-->1) -[6-O-(E)- p-coumaroyl]-alpha-D-glucopyranoside, 3-O-[(E)-3,4,5-trimethoxycinnamoyl]-beta-D-fructofuranosyl-(2-->1) -[6-O-(E)- 3,4,5-trimethoxycinnamoyl]-alpha-D-glucopyranoside, 1-O-{6-O-[3-O-(E,E)-(beta, beta'-bis-sinapoyl)-beta-D-fructofuranosyl]}-alpha- D-glucopyranoside intramolecular ester, 1-O-(E)-p-coumaroyl-(3-O-benzoyl)-beta-D- fructofuranosyl-(2-->1)-[beta-D-glucopyranosyl-(1-->2)]-[6-O-acetyl-beta -D- glucopyranoysl-(1-->3)]-[4-O-(E)-feruloyl]-(6-D-acetyl)-alph a-D- glucopyranoside, 1-O-(E)-p-coumaroyl-(3-O-benzoyl)-beta-D-fructofuranosyl-(2-->1)-[ beta-D- glucopyranosyl-(1-->2)]-[6-O-acetyl-beta-D-glucopyranoside-(1-->3)]-{4-O - [4-O-beta-D-glucopyranosyl-(E)-feruloyl]}-[6-O-(E)-p-coumaroyl+ ++]-alpha- D-glucopyranosyl, respectively, on the basis of chemical and spectral evidence.

Polygalasaponins XLII-XLVI from roots of Polygala glomerata.

Five new oleanane-type saponins, polygalasaponins XLII-XLVI, along with two known saponins were isolated from the roots of Polygala glomerata Lour. The structures of polygalasaponins XLII-XLVI were elucidated as 3-O-beta-D-glucopyranosyl presenegenin 28-O-beta-D-xylopyranosyl-(1-->4)-alpha-L-rhamnopyranosyl- (1-->2)-{4-O-[(E)-3,4-dimethoxycinnamoyl]}-beta-D-fucopyranosyl ester, 3-O-beta-D-glucopyranosyl presenegenin 28-O-beta-D-galactopyranosyl-(1-->4)-beta-D-xylopyranosyl-(1-->4)- alpha-L-rhamnopyranosyl-(1-->2)-[alpha-L-arabinopyranosyl- (1-->3)]-[4-O-(E)-p-methoxycinnamoyl]-beta-D-fucopyranosyl ester, 3-O-beta-D-glucopyranosyl presenegenin 28-O-beta-D-galactopyranosyl-(1-->4)-beta-D-xylopyranosyl-(1-->4)- alpha-L-rhamnopyranosyl-(1-->2)-[beta-D-glucopyranosyl- (1-->3)]-{4-O-[(E)-3,4-dimethoxycinnamoyl]}-beta-D-fucopyranosyl ester, 3-O-beta-D-glucopyranosyl presenegenin 28-O-beta-D-galactopyranosyl-(1-->4)-beta-D-xylopyranosyl-(1-->4)- alpha-L-rhamnopyranosyl-(1-->2)-[6-O- acetyl-beta-D-glucopyranosyl-(1-->3)]-{4-O- [(E)-3,4-dimethoxycinnamoyl]}-beta-D-fucopyranosyl ester, 3-O-beta-D- glucopyranosyl presenegenin 28-O-beta-D-galactopyranosyl-(1-->4)- beta-D-xylopyranosyl-(1-->4)-alpha-L-rhamnopyranosyl- (1-->2)-[6-O-acetyl-beta-D-glucopyranosyl-(1-->3)]-{4-O-[(Z)-3, 4-dimethoxycinnamoyl]}-beta-D-fucopyranosyl ester, respectively, on the basis of spectroscopic and chemical evidence.