Convallaria majalis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA769782 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16268145_1.fastq.gz | Fastqsanger.gz | |||
| SRR16268145_2.fastq.gz | Fastqsanger.gz |
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Project description:Phytochemical examination of Convallaria majalis (Liliaceae) whole plants yielded 15 steroidal glycosides (1-15), including nine new compounds (4-6, 10-15) with a lycotetrose unit. The structures of the new compounds were determined using two-dimensional Nuclear magnetic resonance (NMR) analyses and chemical methods. The isolated compounds were evaluated for cytotoxicity against HL-60 human promyelocytic leukemia cells, A549 human lung adenocarcinoma cells, and HSC-4 and HSC-2 human oral squamous cell carcinoma cell lines. Of these, (25S)-spirost-5-en-3?-yl O-?-d-glucopyranosyl-(1?2)-O-[?-d-xylopyranosyl-(1?3)]-O-?-d-glucopyranosyl-(1?4)-?-d-galactopyranoside (1) exhibited cytotoxic activity against HL-60, A549, HSC-4, and HSC-2 cells with IC50 values ranging from 0.96 to 3.15 ?M. The corresponding furostanol glycoside of 1, (25S)-26-[(?-d-glucopyranosyl)oxy]-22?-hydroxyfurost-5-en-3?-yl O-?-d-glucopyranosyl-(1?2)-O-[?-d-xylopyranosyl-(1?3)]-O-?-d-glucopyranosyl-(1?4)-?-d-galactopyranoside (8), was cytotoxic to the adherent cell lines of A549, HSC-4, and HSC-2 cells with IC50 values of 2.97, 11.04, and 8.25 ?M, respectively. The spirostanol lycotetroside (1) caused necrotic cell death in A549 cells in a dose-dependent manner. Alternatively, the furostanol lycotetroside (8) induced apoptotic cell death in A549 cells in a time-dependent manner, as was evident by morphological observations and flow cytometry analyses.
| S-EPMC5713327 | biostudies-literature
Project description:A fast and efficient selective pressurized liquid extraction (sPLE) method was developed to extract secondary metabolites from complex plant matrix. Convallaria majalis L., a plant producing toxic steroids, was used as proof-of-concept. The method was optimized in the aspects of preheating, dispersant, extraction temperature and solvent, and the use of C18 as in-cell cleanup sorbent. Eight authentic natural steroids with diverse sugar moieties and hydrophobicities were selected as reference analytes and spiked to 0.1 g dried leaves. The extraction performance was evaluated based on the analytes' stability, recovery, matrix effect in the electrospray interface and the level of co-extractives. With the optimal method, the extraction was finished in 10 min. A colorless extract was obtained with recoveries ranging from 63% to 107% and absolute matrix effects ranging from 3% to 27%. The optimized method was validated by extracting 0.1 g, 0.2 g and 0.4 g spiked plant samples; method accuracy and precision were assessed by recoveries and relative standard deviations of the combined extraction-analysis workflow. The method was also tested on soil samples and indicated its suitability for measuring secondary metabolites in multiple environmental matrices. To our knowledge, this is the first time sPLE has been reported to extract plant secondary metabolites from a complex plant matrix, with satisfactory recoveries and low matrix effects. This is also the first time (s)PLE has been reported to extract plant secondary metabolites from soil. We envision the method be coupled with liquid chromatography-electrospray ionization-high resolution mass spectrometry in a standard metabolomics workflow to facilitate plant metabolomics studies.
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Project description:Two new spirostanol sapogenins (5β-spirost-25(27)-en-1β,2β,3β,5β-tetrol 3 and its 25,27-dihydro derivative, (25S)-spirostan-1β,2β,3β,5β-tetrol 4) and four new saponins were isolated from the roots and rhizomes of Convallaria majalis L. together with known sapogenins (isolated from Liliaceae): 5β-spirost-25(27)-en-1β,3β-diol 1, (25S)-spirostan-1β,3β-diol 2, 5β-spirost-25(27)-en-1β,3β,4β,5β-tetrol 5, (25S)-spirostan-1β,3β,4β,5β-tetrol 6, 5β-spirost-25(27)-en-1β,2β,3β,4β,5β-pentol 7 and (25S)-spirostan-1β,2β,3β,4β,5β-pentol 8. New steroidal saponins were found to be pentahydroxy 5-O-glycosides; 5β-spirost-25(27)-en-1β,2β,3β,4β,5β-pentol 5-O-β-galactopyranoside 9, 5β-spirost-25(27)-en-1β,2β,3β,4β,5β-pentol 5-O-β-arabinonoside 11, 5β-(25S)-spirostan-1β,2β,3β,4β,5β-pentol 5-O-galactoside 10 and 5β-(25S)-spirostan-1β,2β,3β,4β,5β-pentol 5-O-arabinoside 12 were isolated for the first time. The structures of those compounds were determined by NMR spectroscopy, including 2D COSY, HMBC, HSQC, NOESY, ROESY experiments, theoretical calculations of shielding constants by GIAO DFT, and mass spectrometry (FAB/LSI HR MS). An attempt was made to test biological activity, particularly as potential chemotherapeutic agents, using in silico methods. A set of 12 compounds was docked to the PDB structures of HER2 receptor and tubulin. The results indicated that diols have a higher affinity to the analyzed targets than tetrols and pentols. Two compounds (25S)-spirosten-1β,3β-diol 1 and 5β-spirost-25(27)-en-1β,2β,3β,4β,5β-pentol 5-O-galactoside 9 were selected for further evaluation of biological activity.
| S-EPMC8158116 | biostudies-literature
Project description:Primary objectives: The primary objective is to investigate circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
Primary endpoints: circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
| 2533916 | ecrin-mdr-crc
Project description:The goals of these studies are to explore the mechanisms that enable extreme physiological plasticity and that may account for evolutionary divergence of adaptive osmotic physiologies among taxa that occupy different osmotic niches. In a common-garden environment, we track physiological and genome expression responses to hypo-osmotic (freshwater) challenge during a time-course of acclimation, and contrast these responses within and between species. We seek to identify mechanisms that facilitate osmotic acclimation that are evolutionarily conserved between basal and derived physiologies, and identify mechanisms that are uniquely derived to enable the extreme osmotic plasticity exhibited by F. heteroclitus. Importantly, previous studies using a comparable experimental design have identified physiological changes and genome expression responses that are adaptive for populations of F. heteroclitus that live in fresh water. As such, this enables us to test whether mechanisms of adaptive micro-evolutionary divergence across osmotic gradients within F. heteroclitus are shared with the mechanisms that account for patterns of macro-evolutionary divergence between F. heteroclitus and F. majalis that we identify in this study. That is, are the targets of micro-evolutionary fine-tuning the same or different as the targets of macro-evolutionary divergence across osmotic boundaries? Population comparisons include between populations from Chesapeake Bay (CB), coastal Virginia (VA), and coastal Georgia (GA).
2013-04-23 | E-MTAB-1551 | biostudies-arrayexpress