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[PMID]: 29208543
[Au] Autor:Gong G; Jiang L; Lin Q; Liu W; He MF; Zhang J; Feng F; Qu W; Xie N
[Ad] Address:Department of Natural Medicinal Chemistry, China Pharmaceutical University, Nanjing 210009, China.
[Ti] Title:In vivo toxic effects of 4-methoxy-5-hydroxy-canthin-6-one in zebrafish embryos via copper dyshomeostasis and oxidative stress.
[So] Source:Comp Biochem Physiol C Toxicol Pharmacol;204:79-87, 2018 Jan.
[Is] ISSN:1532-0456
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dysfunction of copper homeostasis can lead to a host of disorders, which might be toxic sometimes. 4-Methoxy-5-hydroxy-canthin-6-one (CAN) is one of the major constituents from Picrasma quassioides and responsible for its therapeutic effects. In this work, we evaluated the toxic effect of CAN (7.5µM) on zebrafish embryos. CAN treatment decreased survival, delayed hatching time and induced malformations (loss of pigmentation, pericardial edema, as well as hematologic and neurologic abnormalities). Besides, exogenous copper supplementation rescued the pigmentation and cardiovascular defects in CAN-treated embryos. Further spectroscopic studies revealed a copper-chelating activity of CAN. Then its regulation on the expressions of copper homeostasis related genes also be analyzed. In addition, CAN lowered the total activity of SOD, elevated the ROS production and altered the oxidative related genes transcriptions, which led to oxidative stress. In conclusion, we demonstrated that CAN (7.5µM) might exert its toxic effects in zebrafish embryos by causing copper dyshomeostasis and oxidative stress. It will give insight into the risk assessment and prevention of CAN-mediated toxicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180107
[Lr] Last revision date:180107
[St] Status:In-Process

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[PMID]: 29062115
[Au] Autor:Shi Y; Wang R; Zhu X; Xu D; Liu W; Feng F
[Ad] Address:Department of Pharmaceutical Analysis, China Pharmaceutical University, Nanjing, 210009, China.
[Ti] Title:A self-feedback network based on liquid chromatography-quadrupole-time of flight mass spectrometry for system identification of ß-carboline alkaloids in Picrasma quassioides.
[So] Source:Sci Rep;7(1):13841, 2017 Oct 23.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Profiling chemical components in herbs by mass spectrometry is a challenging work because of the lack of standard compounds, especially for position isomers. This paper provides a strategy based on a self-feedback network of mass spectra (MS) data to identify chemical constituents in herbs by liquid chromatography-quadrupole-time of flight mass spectrometry without compound standards. Components sharing same skeleton were screened and all ions were classified into a database. All candidates were connected by the selected bridging ions to establish a primary MS network. Benefited from such a network, it is feasible to characterize sequentially the structures of all diagnostic ions and candidates once single component has been de novo identified. Taking Picrasma quassioides as an example, the primary network of ß-carbolines was established with 65 ions (selected from 76 ß-carbolines), each of which appeared at least in four compounds. Once an alkaloid has been identified, its logical ions could feedback into primary network to build pathways with other unknown compounds. Moreover, the position of the substituent groups could be deduced through the secondary metabolic pathways of alkaloids (plant secondary metabolism). The network therefore can be utilized for identification of unknown compounds and even their position isomers.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171027
[Lr] Last revision date:171027
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-017-13106-8

  3 / 66 MEDLINE  
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[PMID]: 29017159
[Au] Autor:Kong L; Wang B; Yang X; Guo H; Zhang K; Zhu Z; Liu J; Hao D
[Ti] Title:Picrasidine I from Picrasma Quassioides Suppresses Osteoclastogenesis via Inhibition of RANKL Induced Signaling Pathways and Attenuation of ROS Production.
[So] Source:Cell Physiol Biochem;43(4):1425-1435, 2017.
[Is] ISSN:1421-9778
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:BACKGROUND/AIMS: Osteoporosis is a metabolic bone disorder that tortures about millions of people worldwide. Recent study demonstrated agents derived from picrasma quassioides is a promising drug for targets multiple signaling pathways. However its potential in treatment of bone loss has not been fully understood. METHODS: The bone marrow macrophages (BMMs) were cultured and induced with M-CSF and RANKL followed by picrasidine I (PI) treatment. Then the effects of PI on osteoclast formation were evaluated by counting tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. Moreover, effects of PI on bone resorption activity of mature osteoclast were studied through bone resorption pit counting and actin ring structure analysis. Further, the involved potential signaling pathways cross-talking were investigated by performed Western blotting and quantitative real-time PCR examination. RESULTS: Results demonstrated PI strongly inhibited RANKL induced osteoclast formation from its precursors. Mechanistically, the inhibitory effect of PI on osteoclast differentiation was due to the suppression of osteoclastogenic transcription factors, c-Fos and NFATc1. Moreover, PI markedly blocked the RANKL-induced osteoclastogenesis by attenuating MAPKs and NF-κB signaling pathways. In addition, PI decreased the ROS generation in osteoclast and osteoblast. CONCLUSION: Taken together our data demonstrate that PI has antiosteoclastogenic effect by inhibiting inflammation induced activation of MAPKs, NF-κB and ROS generation followed by suppressing the gene expression of c-Fos and NFATc1 in osteoclast precursors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171119
[Lr] Last revision date:171119
[St] Status:In-Process
[do] DOI:10.1159/000481874

  4 / 66 MEDLINE  
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[PMID]: 28962866
[Au] Autor:Miao X; You J; Wang J; Chen Y
[Ad] Address:Hubei Province Key Laboratory of Biotechnology of Chinese Traditional Medicine, Hubei Collaborative Innovation Center for Green Transformation of Bio-resources, Hubei University, Wuhan, Hubei 430062, China.
[Ti] Title:In vitro metabolism of 4, 5-dimethoxycanthin-6-one by human liver microsomes and its inhibition on human CYP1A2.
[So] Source:Life Sci;190:46-51, 2017 Dec 01.
[Is] ISSN:1879-0631
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:AIMS: P. quassioides is a traditional Chinese medicine used for the treatment of gastroenteritis, snakebite, infection and hypertension in China. 4, 5-dimethoxycanthin-6-one is one of the main active canthinone alkaloid isolated from P. quassioides. The aim of this work was to identify the cytochrome P (CYP) 450 enzymes responsible for the metabolism of 4, 5-dimethoxycanthin-6-one (DCO) and to evaluate the inhibitory effect of DCO on CYP activity in human liver microsomes (HLM) in vitro. MATERIALS AND METHODS: the CYP isoforms responsible for DCO metabolism and the inhibitory effects of DCO on CYP activity was studied in HLM. KEY FINDINGS: The in vitro metabolic enzyme of DCO was CYP3A4 (mediated the formation of metabolites M1-M5), CYP2C9 (mediated the formation of metabolites M1-M3, M6 and M8) and CYP2D6 (mediated the formation of metabolite M3) in HLM. Furthermore, the present work found that DCO uncompetitively inhibited CYP1A2-mediated phenacetin O-deethylation with an IC value of 1.7µM and a Ki value of 2.6µM. SIGNIFICANCE: The results suggested that the metabolic interaction should be existed when the substrate drugs of CYP1A2 were co-administered with DCO or traditional Chinese medicine containing it, such as the extract of P. quassioides and Kumu injection.
[Mh] MeSH terms primary: Carbolines/administration & dosage
Cytochrome P-450 CYP1A2 Inhibitors/administration & dosage
Cytochrome P-450 CYP1A2/drug effects
Microsomes, Liver/drug effects
Picrasma/chemistry
[Mh] MeSH terms secundary: Carbolines/metabolism
Carbolines/pharmacology
Cytochrome P-450 CYP1A2/metabolism
Cytochrome P-450 CYP1A2 Inhibitors/metabolism
Cytochrome P-450 CYP1A2 Inhibitors/pharmacology
Cytochrome P-450 Enzyme System/drug effects
Cytochrome P-450 Enzyme System/metabolism
Humans
In Vitro Techniques
Inhibitory Concentration 50
Microsomes, Liver/enzymology
Microsomes, Liver/metabolism
Plant Extracts/administration & dosage
Plant Extracts/metabolism
Plant Extracts/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (4,5-dimethoxycanthin-6-one); 0 (Carbolines); 0 (Cytochrome P-450 CYP1A2 Inhibitors); 0 (Plant Extracts); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.14.1 (CYP1A2 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP1A2)
[Em] Entry month:1710
[Cu] Class update date: 171030
[Lr] Last revision date:171030
[Js] Journal subset:IM
[Da] Date of entry for processing:171001
[St] Status:MEDLINE

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[PMID]: 28427809
[Au] Autor:Yamashita N; Kondo M; Zhao S; Li W; Koike K; Nemoto K; Kanno Y
[Ad] Address:Department of Molecular Toxicology, Faculty of Pharmaceutical Sciences, Toho University, Miyama 2-2-1, Funabashi, Chiba 274-8510, Japan.
[Ti] Title:Picrasidine G decreases viability of MDA-MB 468 EGFR-overexpressing triple-negative breast cancer cells through inhibition of EGFR/STAT3 signaling pathway.
[So] Source:Bioorg Med Chem Lett;27(11):2608-2612, 2017 06 01.
[Is] ISSN:1464-3405
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Targeted therapy is unavailable for treating patients with triple-negative breast cancer (TNBC), which accounts for approximately 15% of all breast cancers. Overexpression of epidermal growth factor receptor (EGFR) is observed in approximately 30-60% of TNBCs. Therefore, developing novel strategies for inhibiting EGFR signaling is required. In the present study, a natural compound library was screened to identify molecules that target TNBCs that overexpress EGFR. Picrasidine G (PG), a naturally occurring dimeric alkaloid produced by Picrasma quassioides, decreased the viability of the MDA-MB 468 cell line (TNBC ) compared with other breast cancer cell lines. PG treatment increased markers of apoptosis, including chromatin condensation, sub-G1 population, cleavage of caspase 3 and cleavage of poly (ADP-ribose) polymerase (PARP). PG inhibited the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and inhibited transcription of the STAT3-target gene encoding survivin. Further, PG inhibited EGF-induced STAT3 phosphorylation but not interleukin-6 (IL-6)-induced STAT3 phosphorylation. These results suggest that PG may contribute to the development of targeted therapy of patients with EGFR-overexpressing TNBC.
[Mh] MeSH terms primary: Alkaloids/chemistry
Carbolines/toxicity
Receptor, Epidermal Growth Factor/metabolism
STAT3 Transcription Factor/metabolism
Signal Transduction/drug effects
[Mh] MeSH terms secundary: Alkaloids/toxicity
Apoptosis/drug effects
Carbolines/chemistry
Caspase 3/metabolism
Cell Line, Tumor
Cell Survival/drug effects
Female
G1 Phase Cell Cycle Checkpoints/drug effects
Humans
Interleukin-6/pharmacology
Phosphorylation/drug effects
Poly(ADP-ribose) Polymerases/metabolism
Triple Negative Breast Neoplasms/metabolism
Triple Negative Breast Neoplasms/pathology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Alkaloids); 0 (Carbolines); 0 (Interleukin-6); 0 (STAT3 Transcription Factor); 0 (picrasidine G); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.22.- (Caspase 3)
[Em] Entry month:1708
[Cu] Class update date: 171124
[Lr] Last revision date:171124
[Js] Journal subset:IM
[Da] Date of entry for processing:170422
[St] Status:MEDLINE

  6 / 66 MEDLINE  
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[PMID]: 28258983
[Au] Autor:Miao X; Wang J; Chen Y
[Ad] Address:Hubei Province Key Laboratory of Biotechnology of Chinese Traditional Medicine, Hubei Collaborative Innovation Center for Green Transformation of Bio-resources, Hubei University, Wuhan 430062, China.
[Ti] Title:Pharmacokinetics and tissue distribution of 4,5-dimethoxycanthin-6-one and its major metabolites in rats.
[So] Source:J Pharm Biomed Anal;139:22-29, 2017 May 30.
[Is] ISSN:1873-264X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:4,5-Dimethoxycanthin-6-one and 5-hydroxy-4-methoxycanthin-6-one are the active ingredients of P. quassiodes. In the present work, a LC-MS/MS method was developed for the determination of 4,5-dimethoxycanthin-6-one and its major metabolites 5-hydroxy-4-methoxycanthin-6-one (M1) and 4-hydroxy-5-methoxycanthin-6-one (M2) in rat plasma and tissues, and applied to study their pharmacokinetics and tissue distribution after intramuscular administration of 4,5-dimethoxycanthin-6-one to rats. By protein precipitation with methanol for plasma samples and liquid-liquid extraction with ethyl acetate for tissue samples, the analytes were separated on an ODS C column with a mobile phase consisted of methanol and water (0.1% formic acid), and quantified by a MS detector in positive multiple reaction monitoring (MRM) mode. MS transitions were m/z 281.0→167.1 for 4,5-dimethoxycanthin-6-one, m/z 267.0→168.1 for M1 and M2, m/z 251.0→195.1 for 3-methylcanthin-2,6-dione (IS). The pharmacokinetic results indicate that 4,5-dimethoxycanthin-6-one is absorbed rapidly (T =5.4-6.4min), distributed rapidly and widely in the order of liver>kidney≈lung≈large intestine≈small intestine, and eliminated quickly (t =64.9-77.7min) following the intramuscular administration. Furthermore, M1 and M2 were detected only in rat plasma and liver at the indicated times after the intramuscular administration.
[Mh] MeSH terms primary: Carbolines/blood
Carbolines/pharmacokinetics
Drugs, Chinese Herbal/pharmacokinetics
Picrasma
[Mh] MeSH terms secundary: Animals
Carbolines/administration & dosage
Chromatography, High Pressure Liquid/methods
Drugs, Chinese Herbal/administration & dosage
Drugs, Chinese Herbal/metabolism
Injections, Intramuscular
Male
Random Allocation
Rats
Rats, Sprague-Dawley
Tandem Mass Spectrometry/methods
Tissue Distribution/drug effects
Tissue Distribution/physiology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (5-methoxycanthin-6-one); 0 (Carbolines); 0 (Drugs, Chinese Herbal)
[Em] Entry month:1708
[Cu] Class update date: 170803
[Lr] Last revision date:170803
[Js] Journal subset:IM
[Da] Date of entry for processing:170305
[St] Status:MEDLINE

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[PMID]: 27237303
[Au] Autor:Fan HX; Zhou ZQ; Peng J; Wu BJ; Chen HR; Bao XF; Mu ZQ; Jiao WH; Yao XS; Gao H
[Ad] Address:a Institute of Traditional Chinese Medicine and Natural Products, College of Pharmacy, Jinan University , Guangzhou , P.R. China.
[Ti] Title:A microbial model of mammalian metabolism: biotransformation of 4,5-dimethoxyl-canthin-6-one using Cunninghamella blakesleeana CGMCC 3.970.
[So] Source:Xenobiotica;47(4):284-289, 2017 Apr.
[Is] ISSN:1366-5928
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:1. A filamentous fungus, Cunninghamella blakesleeana CGMCC 3.970, was applied as a microbial system to mimic mammalian metabolism of 4,5-dimethoxyl-canthin-6-one (1). Compound 1 belongs to canthin-6-one type alkaloids, which is a major bioactive constituent of a traditional Chinese medicine (the stems of Picrasma quassioides). 2. After 72 h of incubation in potato dextrose broth, 1 was metabolized to seven metabolites as follows: 4-methoxyl-5-hydroxyl-canthin-6-one (M1), 4-hydroxyl-5-methoxyl-canthin-6-one (M2), canthin-6-one (M3), canthin-6-one N-oxide (M4), 10-hydroxyl-4,5-dimethoxyl-canthin-6-one (M5), 1-methoxycarbonl-ß-carboline (M6), and 4-methoxyl-5-O-ß-D-glucopyranosyl-canthin-6-one (M7). 3. The structures of metabolites were determined using spectroscopic analyses, chemical methods, and comparison of NMR data with those of known compounds. Among them, M7 was a new compound. 4. The metabolic pathways of 1 were proposed, and the metabolic processes involved phase I (O-demethylation, dehydroxylation, demethoxylation, N-oxidation, hydroxylation, and oxidative ring cleavage) and phase II (glycosylation) reactions. 5. This was the first research on microbial transformation of canthin-6-one alkaloid, which could be a useful microbial model for producing the mammalian phase I and phase II metabolites of canthin-6-one alkaloids. 6. 1, M1-M5, and M7 are canthin-6-one alkaloids, whereas M6 belongs to ß-carboline type alkaloids. The strain of Cunninghamella blakesleeana can supply an approach to transform canthin-6-one type alkaloids into ß-carboline type alkaloids.
[Mh] MeSH terms primary: Biotransformation
Carbolines/metabolism
Cunninghamella/metabolism
Indole Alkaloids/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Carbolines); 0 (Indole Alkaloids); 3FK17S759N (canthin-6-one)
[Em] Entry month:1707
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:IM
[Da] Date of entry for processing:160531
[St] Status:MEDLINE
[do] DOI:10.1080/00498254.2016.1184774

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[PMID]: 27958735
[Au] Autor:Zhao S; Kanno Y; Li W; Sasaki T; Zhang X; Wang J; Cheng M; Koike K; Nemoto K; Li H
[Ad] Address:College of Life Science, Northeast Forestry University , Harbin 150040, People's Republic of China.
[Ti] Title:Identification of Picrasidine C as a Subtype-Selective PPARα Agonist.
[So] Source:J Nat Prod;79(12):3127-3133, 2016 Dec 23.
[Is] ISSN:1520-6025
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Picrasidine C (1), a dimeric ß-carboline-type alkaloid isolated from the root of Picrasma quassioides, was identified to have PPARα agonistic activity by a mammalian one-hybrid assay from a compound library. Among the PPAR subtypes, 1 selectively activated PPARα in a concentration-dependent manner. Remarkably, 1 also promoted PPARα transcriptional activity by a peroxisome proliferator response element-driven luciferase reporter assay. Furthermore, 1 induced the expression of PPARα-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARα, PDK4, and ABCA1, which was abrogated by the PPARα antagonist MK-886, indicating that the effect of 1 was dependent on PPARα activation. This is the first report to demonstrate 1 to be a subtype-selective PPARα agonist with potential application in treating metabolic diseases, such as hyperlipidemia, atherosclerosis, and hypercholesterolemia.
[Mh] MeSH terms primary: Alkaloids/isolation & purification
Alkaloids/pharmacology
Carbolines/isolation & purification
Carbolines/pharmacology
PPAR alpha/agonists
Picrasma/chemistry
[Mh] MeSH terms secundary: Alkaloids/chemistry
Animals
Atherosclerosis/drug therapy
Carbolines/chemistry
Cholesterol/metabolism
Glucose/metabolism
Hypercholesterolemia/drug therapy
Indoles/pharmacology
Lipid Metabolism
Lipids
Mice
Molecular Structure
PPAR alpha/genetics
Transcription Factors/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Alkaloids); 0 (Carbolines); 0 (Indoles); 0 (Lipids); 0 (PPAR alpha); 0 (Transcription Factors); 080626SQ8C (MK-886); 94HMA1I78O (norharman); 97C5T2UQ7J (Cholesterol); IY9XDZ35W2 (Glucose)
[Em] Entry month:1705
[Cu] Class update date: 170503
[Lr] Last revision date:170503
[Js] Journal subset:IM
[Da] Date of entry for processing:161214
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jnatprod.6b00883

  9 / 66 MEDLINE  
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[PMID]: 27575477
[Au] Autor:Win NN; Ito T; Win YY; Ngwe H; Kodama T; Abe I; Morita H
[Ad] Address:Institute of Natural Medicine, University of Toyama, 2630-Sugitani, Toyama 930-0194, Japan; Department of Chemistry, University of Yangon, Yangon 11041, Myanmar. Electronic address: nwetwin2012@gmail.com.
[Ti] Title:Quassinoids: Viral protein R inhibitors from Picrasma javanica bark collected in Myanmar for HIV infection.
[So] Source:Bioorg Med Chem Lett;26(19):4620-4624, 2016 10 01.
[Is] ISSN:1464-3405
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Viral protein R (Vpr) is an accessory protein that plays important roles in the viral pathogenesis of Human Immunodeficiency Virus-1 (HIV-1). An assay for anti-Vpr activity, using TREx-HeLa-Vpr cells, is a promising strategy to discover Vpr inhibitors. The anti-Vpr assay revealed that the CHCl3-soluble extract of Picrasma javanica bark possesses potent anti-Vpr activity. Furthermore, studies of quassinoids (1-15) previously isolated from the extract demonstrated that all of the tested quassinoids exhibit anti-Vpr activity. Among the tested compounds, javanicin I (15) exhibited the most potent anti-Vpr activity ((***)p <0.001) in comparing with that of the positive control, damnacanthal. The structure-activity relationships of the active quassinoids suggested that the presence of a methyl group at C-13 in the 2,12,14-triene-1,11,16-trione-2,12-dimethoxy-18-norpicrasane quassinoids is the important factor for the potent inhibitory effect in TREx-HeLa-Vpr cells.
[Mh] MeSH terms primary: Anti-HIV Agents/therapeutic use
Gene Products, vpr/antagonists & inhibitors
HIV Infections/drug therapy
Picrasma/chemistry
Plant Bark/chemistry
Quassins/pharmacology
[Mh] MeSH terms secundary: Anti-HIV Agents/chemistry
Anti-HIV Agents/pharmacology
HeLa Cells
Humans
Myanmar
Quassins/chemistry
Structure-Activity Relationship
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Anti-HIV Agents); 0 (Gene Products, vpr); 0 (Quassins)
[Em] Entry month:1708
[Cu] Class update date: 171122
[Lr] Last revision date:171122
[Js] Journal subset:IM
[Da] Date of entry for processing:160831
[St] Status:MEDLINE

  10 / 66 MEDLINE  
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[PMID]: 27494664
[Au] Autor:Xu J; Xiao D; Lin QH; He JF; Liu WY; Xie N; Feng F; Qu W
[Ti] Title:Cytotoxic Tirucallane and Apotirucallane Triterpenoids from the Stems of Picrasma quassioides.
[So] Source:J Nat Prod;79(8):1899-910, 2016 Aug 26.
[Is] ISSN:1520-6025
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Phytochemical investigation on the stems of Picrasma quassioides led to the isolation of a novel compound, picraquassin A (1), with an unprecedented 21,24-cycloapotirucallane skeleton, and four new apotirucallane-type triterpenoids (2-5), together with 15 new tirucallane-type triterpenoids (6-20) and 10 known tirucallane-type triterpenoids (21-30). To our knowledge, this is the first report demonstrating the presence of apotirucallane-type triterpenoids in the genus Picrasma. The structures of the new compounds were determined based on spectroscopic data interpretation. Cytotoxicities of the isolated compounds were evaluated using three human cancer cell lines, MKN-28, A-549, and MCF-7. Compound 2 exhibited the most potent activity against MKN-28 cells with an IC50 value of 2.5 µM. Flow cytometry and Western blot analysis revealed that 2 induces the apoptosis of MKN-28 cells via activating caspase-3/-9, while increasing Bax and Bad and decreasing Bcl-2 expression levels.
[Mh] MeSH terms primary: Antineoplastic Agents, Phytogenic
Drugs, Chinese Herbal
Picrasma/chemistry
Plant Stems/chemistry
Triterpenes
[Mh] MeSH terms secundary: Antineoplastic Agents, Phytogenic/chemistry
Antineoplastic Agents, Phytogenic/classification
Antineoplastic Agents, Phytogenic/isolation & purification
Antineoplastic Agents, Phytogenic/pharmacology
Drug Screening Assays, Antitumor
Drugs, Chinese Herbal/chemistry
Drugs, Chinese Herbal/isolation & purification
Drugs, Chinese Herbal/pharmacology
Inhibitory Concentration 50
Molecular Structure
Nuclear Magnetic Resonance, Biomolecular
Triterpenes/chemistry
Triterpenes/classification
Triterpenes/isolation & purification
Triterpenes/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents, Phytogenic); 0 (Drugs, Chinese Herbal); 0 (Triterpenes); 0 (picraquassin A); 0 (picraquassin B)
[Em] Entry month:1705
[Cu] Class update date: 170502
[Lr] Last revision date:170502
[Js] Journal subset:IM
[Da] Date of entry for processing:160806
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jnatprod.5b01137


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