lignans and Leukemia

lignans has been researched along with Leukemia* in 21 studies

Other Studies

21 other study(ies) available for lignans and Leukemia

ArticleYear
Honokiol Provides Cardioprotection from Myocardial Ischemia/Reperfusion Injury (MI/RI) by Inhibiting Mitochondrial Apoptosis via the PI3K/AKT Signaling Pathway.
    Cardiovascular therapeutics, 2022, Volume: 2022

    Honokiol can reduce the MI/RI-induced cTnT and CK-MB levels, apoptosis index, and mitochondrial swelling in cardiomyocytes via activating the PI3K/AKT signaling pathway.. Honokiol provides cardiac protection from MI/RI by suppressing mitochondrial apoptosis through the PI3K/AKT signaling pathway.

    Topics: Animals; Apoptosis; Biphenyl Compounds; Humans; Leukemia; Lignans; Lymphoma, B-Cell; Male; Mice; Mice, Inbred C57BL; Myocardial Reperfusion Injury; Myocytes, Cardiac; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Signal Transduction

2022
Phyllanthin inhibits MOLT-4 leukemic cancer cell growth and induces apoptosis through the inhibition of AKT and JNK signaling pathway.
    Journal of biochemical and molecular toxicology, 2021, Volume: 35, Issue:6

    Topics: Apoptosis; Cell Line, Tumor; Cell Proliferation; Humans; Leukemia; Lignans; MAP Kinase Kinase 4; Proto-Oncogene Proteins c-akt; Signal Transduction

2021
The augmented anticancer potential of AP9-cd loaded solid lipid nanoparticles in human leukemia Molt-4 cells and experimental tumor.
    Chemico-biological interactions, 2016, Jan-25, Volume: 244

    AP9-cd, a novel lignan composition from Cedrus deodara has significant anticancer potential, and to further enhance its activity, it was lucratively encumbered into solid lipid nanoparticles (SLNs). These nanoparticles were formulated by micro-emulsion technique with 70% drug trap competence. AP9-cd-SLNs were regular, solid, globular particles in the range of 100-200 nm, which were confirmed by electron microscopic studies. Moreover, AP9-cd-SLNs were found to be stable for up to six months in terms of color, particle size, zeta potential, drug content and entrapment. AP9-cd-SLNs have 30-50% higher cytotoxic and apoptotic potential than the AP9-cd alone. The augmented anticancer potential of AP9-cd-SLNs was observed in cytotoxic IC50 value, apoptosis signaling cascade and in Ehrlich ascites tumor (EAT) model. AP9-cd-SLNs induce apoptosis in Molt-4 cells via both intrinsic and extrinsic pathway. Moreover, the dummy nanoparticles (SLNs without AP9-cd) did not have any cytotoxic effect in cancer as well as in normal cells. Consequently, SLNs of AP9-cd significantly augment the apoptotic and antitumor potential of AP9-cd. The present study provides a podium for ornamental the remedial latent via novel delivery systems like solid lipid nanoparticles.

    Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Cedrus; Cell Line, Tumor; Cell Proliferation; Dose-Response Relationship, Drug; Humans; Leukemia; Lignans; Lipids; Mice; Mice, Inbred BALB C; Nanoparticles; Neoplasms, Experimental; Particle Size; Structure-Activity Relationship; Surface Properties

2016
Pro-Apoptotic Activity of New Honokiol/Triphenylmethane Analogues in B-Cell Lymphoid Malignancies.
    Molecules (Basel, Switzerland), 2016, Jul-30, Volume: 21, Issue:8

    Honokiol and triphenylmethanes are small molecules with anti-tumor properties. Recently, we synthesized new honokiol analogues (HAs) that possess common features of both groups. We assessed the anti-tumor effectiveness of HAs in B-cell leukemia/lymphoma cells, namely in chronic lymphocytic leukemia (CLL) cells ex vivo and in pre-B-cell acute lymphoblastic leukemia (Nalm-6), Burkitt lymphoma (BL; Raji), diffuse large B-cell lymphoma (DLBCL; Toledo) and multiple myeloma (MM; RPMI 8226) cell lines. Four of these compounds appeared to be significantly active against the majority of cells examined, with no significant impact on healthy lymphocytes. These active HAs induced caspase-dependent apoptosis, causing significant deregulation of several apoptosis-regulating proteins. Overall, these compounds downregulated Bcl-2 and XIAP and upregulated Bax, Bak and survivin proteins. In conclusion, some of the HAs are potent tumor-selective inducers of apoptosis in ex vivo CLL and in BL, DLBCL and MM cells in vitro. Further preclinical studies of these agents are recommended.

    Topics: Antineoplastic Agents; Apoptosis; Apoptosis Regulatory Proteins; Biphenyl Compounds; Cell Line, Tumor; Cell Proliferation; Cell Survival; Drug Screening Assays, Antitumor; Gene Expression Regulation, Neoplastic; Humans; Leukemia; Lignans; Lymphoma; Multiple Myeloma; Trityl Compounds

2016
Synthesis of tetrahydrohonokiol derivates and their evaluation for cytotoxic activity against CCRF-CEM leukemia, U251 glioblastoma and HCT-116 colon cancer cells.
    Molecules (Basel, Switzerland), 2014, Jan-20, Volume: 19, Issue:1

    Biphenyl neolignans such as honokiol and magnolol, which are the major active constituents of the Asian medicinal plant Magnolia officinalis, are known to exert a multitude of pharmacological and biological activities. Among these, cytotoxic and tumor growth inhibitory activity against various tumour cell lines are well-documented. To further elucidate the cytotoxic effects of honokiol derivatives, derivatizations were performed using tetrahydrohonokiol as a scaffold. The derivatizations comprised the introduction of functional groups, e.g., nitro and amino groups, as well as alkylation. This way, 18 derivatives, of which 13 were previously undescribed compounds, were evaluated against CCRF-CEM leukemia cells, U251 glioblastoma and HCT-116 colon cancer cells. The results revealed no significant cytotoxic effects in any of the three tested cell lines at a test concentration of 10 µM.

    Topics: Antineoplastic Agents, Phytogenic; Biphenyl Compounds; Cell Survival; Colonic Neoplasms; Drug Screening Assays, Antitumor; Glioblastoma; HCT116 Cells; Humans; Inhibitory Concentration 50; Leukemia; Lignans; Methylation; Microwaves

2014
[Honokiol inhibits the invasion and angiogenesis of U937 leukemia cells].
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology, 2014, Volume: 30, Issue:2

    To investigate the inhibiting effect of Honokiol (HNK) on the invasion and angiogenesis in U937 leukemia cells and the molecular mechanism.. After treated with different concentrations of HNK, the growth inhibition rate of U937 cells was determined by MTT assay, and for the adhesion and invasion abilities were assessed using cell matrix adhesion technique and Transwell(TM); assay, respectively. VEGF, VEGFR1 and MMP-9 mRNA expression levels were detected by real-time quantitative RT-PCR (qRT-PCR). VEGF protein levels were determined by ELISA.. HNK could significantly inhibit the proliferation of U937 cells in a time- and dose-dependent manner. The adhesion and invasion abilities of U937 cells were suppressed after treated with a low concentration of HNK. The expressions of VEGF, VEGFR1 and MMP-9 were down-regulated by HNK in a dose-dependent manner.. HNK can inhibit the invasion and angiogenesis of U937 cells via down-regulating VEGF, VEGFR1 and MMP-9 expressions.

    Topics: Antineoplastic Agents; Biphenyl Compounds; Cell Adhesion; Cell Line, Tumor; Cell Proliferation; Dose-Response Relationship, Drug; Gene Expression Regulation, Neoplastic; Humans; Leukemia; Lignans; Matrix Metalloproteinase 9; Neoplasm Invasiveness; Neovascularization, Pathologic; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-1

2014
HJC, a new arylnaphthalene lignan isolated from Justicia procumbens, causes apoptosis and caspase activation in K562 leukemia cells.
    Journal of pharmacological sciences, 2014, Volume: 125, Issue:4

    The aim of this study is to investigate whether HJC, isolated from Justicia procumbens for the first time, can suppress the proliferation and induce apoptosis of human leukemia K562 cells and finally clarify its related mechanism. The chemical structure of HJC was validated by LC-ESI-MS/MS, cytotoxicity was assayed using MTT, and apoptosis was investigated by flow cytometry. These assays indicated that HJC remarkably inhibited the growth in K562 cells by decreasing cell proliferation, reducing the SOD activity, enhancing ROS levels and inducing apoptosis. Activation of caspase-3 indicated that HJC may be inducing intrinsic and extrinsic apoptosis pathways and that HJC-induced apoptosis was caspase-dependent. This study suggests that HJC is a high-potency anti-tumor agent, and it induces apoptosis through a caspase-dependent pathway in human leukemia K562 cells. It also presents a potential alternative to leukemia therapy.

    Topics: Acanthaceae; Antineoplastic Agents, Phytogenic; Apoptosis; Benzodioxoles; Caspase 3; Cell Transformation, Neoplastic; Depression, Chemical; Enzyme Activation; HL-60 Cells; Humans; K562 Cells; Leukemia; Lignans; Phytotherapy; Reactive Oxygen Species; Superoxide Dismutase

2014
Honokiol induces caspase-independent paraptosis via reactive oxygen species production that is accompanied by apoptosis in leukemia cells.
    Biochemical and biophysical research communications, 2013, Jan-18, Volume: 430, Issue:3

    Our previous report has shown that honokiol (HNK), a constituent of Magnolia officinalis, induces a novel form of non-apoptotic programmed cell death in human leukemia NB4 and K562 cells. In this study, we further explored the relationship between the cell death pathway and cytoplasmic vacuolization and studied the underlying mechanism of leukemia cell death mediated by honokiol. The results showed that low concentrations of honokiol activated an novel alternative cell death fitted the criteria of paraptosis, such as cytoplasmic vacuolization derived from endoplasmic reticulum swelling, lack of caspase activation, and lack of apoptotic morphology. Results further indicated that the cell death was time- and concentration-dependent. In addition, honokiol-induced paraptosis did not involve membrane blebbing, chromatin condensation and phosphatidylserine exposure at the outer of the plasma membrane. The mechanism of the cell death may be associated, at least in part, with the increased generation of reactive oxygen species. Further analysis showed that honokiol induces cell death predominantly via paraptosis and to a certain extent via apoptosis in NB4 cells, and predominantly via apoptosis and to a certain extent via paraptosis in K562 cells. These observations suggest that cell death occurs via more than one pathway in leukemia cells and targeting paraptosis may be an alternative and promising avenue for honokiol in leukemia therapy.

    Topics: Apoptosis; Biphenyl Compounds; Caspases; Cell Line, Tumor; Cell Membrane; Cytoplasm; Endoplasmic Reticulum; Humans; Leukemia; Lignans; Metabolic Networks and Pathways; Necrosis; Phosphatidylserines; Reactive Oxygen Species; Vacuoles

2013
[Anti-tumor effect of tanshinone II A, tetrandrine, honokiol, curcumin, oridonin and paeonol on leukemia cell lines].
    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2012, Volume: 43, Issue:3

    To study the anti-tumor effect of tanshinon II A, tetrandrine, honokiol, curcumin, oridonin and paeonol on leukemia cell lines SUP-B15, K562, CEM, HL-60 and NB4.. To study the anti-tumor effect of tanshinone II A, tetrandrine, honokiol, curcumin, The leukemia cell lines were exposed to the six Chinese herbal components for 96 hours. The proliferative inhibitory effects were detected with MTT and described by IC50 value.. Tanshinone II A inhibited the proliferations of SUP-B15, K562, CEM, HL-60 and NB4 cell lines, with HL-60 showing the least impact. Tetrandrine, honokiol, curcumin and oridonin inhibited the proliferations of SUP-B15, K562, CEM, HL-60 and NB4 cell lines and there was no significant difference between the cell lines. Paeonol did not have significant inhibitory effect on leukemia cell lines.. Tetrandrine, honokiol, curcumin and oridonin inhibit the proliferation of five cell lines SUP-B15, K562, CEM, HL-60, NB4, and the effects are similar, which means that their anticancer effects are quite broad. Tanshinone II A has better anti-leukemia effects on SUP-B15, K562, CEM, NB4 than on HL-60. The effect of paeonol against leukemia cell lines is poor.

    Topics: Abietanes; Acetophenones; Antineoplastic Agents, Phytogenic; Benzylisoquinolines; Biphenyl Compounds; Cell Line, Tumor; Cell Proliferation; Curcumin; Diterpenes, Kaurane; Drugs, Chinese Herbal; HL-60 Cells; Humans; K562 Cells; Leukemia; Lignans; Plants, Medicinal

2012
Larrealignans A and B, novel lignan glycosides from the aerial parts of Larrea tridentata.
    Chemical & pharmaceutical bulletin, 2011, Volume: 59, Issue:12

    Two new lignan glycosides, named larrealignans A (1) and B (2), and a known lignan (3) were isolated from the aerial parts of Larrea tridentata (Zygophyllaceae). The structures of 1 and 2 were determined on the basis of spectroscopic analysis and the results of hydrolytic cleavage. The isolated compounds (1-3) and aglycones (1a, 2a) of 1 and 2 were evaluated for their cytotoxic activities against HL-60 human leukemia cells.

    Topics: Antineoplastic Agents, Phytogenic; Drug Screening Assays, Antitumor; HL-60 Cells; Humans; Larrea; Leukemia; Lignans; Plant Components, Aerial; Spectrum Analysis

2011
Sesamin inhibits bacterial formylpeptide-induced inflammatory responses in a murine air-pouch model and in THP-1 human monocytes.
    The Journal of nutrition, 2010, Volume: 140, Issue:2

    The reaction of human leukocytes to chemoattractants is an important component of the host immune response and also plays a crucial role in the development of inflammation. Sesamin has been shown to inhibit lipid peroxidation and regulate cytokine production. In this study, we examined the effect of sesamin on inflammatory responses elicited by the bacterial chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (fMLF) in vitro and in vivo and explored the mechanisms involved. fMLF is recognized by a human G protein-coupled receptor formyl peptide receptor (FPR) on phagocytic leukocytes. Sesamin at concentrations between 12.5 and 50 micromol/L inhibited fMLF-induced chemotaxis of human monocyte cell line THP-1 differentiated with dibutyryl cyclic AMP (P < 0.01). Similarly, sesamin inhibited FPR-transfected rat basophilic leukemia cell [epitope-tagged human FPR (ETFR) cell] migration toward fMLF (P < 0.01). In fMLF-induced inflammation in a murine air-pouch model, intraperitoneal administration of sesamin (12 mgkg(-1)d(-1) for 2 d) suppressed leukocyte infiltration into the air pouch induced by fMLF [(62.89 +/- 7.93) x 10(4) vs. (19.67 +/- 4.43) x 10(4) cells/air pouch; n = 9; P < 0.001]. Ca(2+) mobilization and mitogen-activated protein kinase extracellular signal-regulated kinase (ERK1/2) activation are involved in fMLF-induced leukocyte migration. Pretreatment of ETFR cells with sesamin inhibited fMLF-induced ERK1/2 phosphorylation in a dose-dependent manner but did not affect fMLF-induced Ca(2+) flux. Electrophoretic mobility shift assay showed that pretreatment of THP-1 cells with sesamin dose dependently inhibited fMLF-induced nuclear factor-kappaB (NF-kappaB) activation. These results suggest that sesamin inhibits leukocyte activation by fMLF through ERK1/2- and NF-kappaB-related signaling pathways and thus is a potential compound for the management of inflammatory diseases.

    Topics: Animals; Anti-Inflammatory Agents; Bacteria; Basophils; Bucladesine; Calcium; Cell Line; Cell Line, Tumor; Chemotaxis, Leukocyte; Dioxoles; Dose-Response Relationship, Drug; Humans; Inflammation; Leukemia; Leukemic Infiltration; Lignans; Mice; Mice, Inbred C57BL; Mitogen-Activated Protein Kinase 1; Models, Animal; Monocytes; N-Formylmethionine Leucyl-Phenylalanine; NF-kappa B; Phosphorylation; Phytotherapy; Plant Extracts; Rats; Receptors, Formyl Peptide; Sesamum; Signal Transduction

2010
Honokiol induces paraptosis and apoptosis and exhibits schedule-dependent synergy in combination with imatinib in human leukemia cells.
    Toxicology mechanisms and methods, 2010, Volume: 20, Issue:5

    Honokiol, an active component isolated and purified from Chinese traditional herb magnolia, has been shown to inhibit growth and induce apoptosis in different cancer cell lines. This study shows that honokiol can induce a cell death distinct from apoptosis at lower concentrations. The death was characterized by cytoplasmic vacuolization with the endoplasmic reticulum swelling and accompanied by apoptosis at higher concentrations in NB4 and K562 cells. The two death processes may be in sequence at lower concentrations and in parallel with the increase of honokiol concentration. Membrane-associated cytotoxicity was involved in honokiol-induced paraptosis and apoptosis. Furthermore, honokiol inhibited concentration-dependent cell adhesion to extracellular matrix for NB4 cells. In addition, the cytotoxicity of honokiol combined treatment with imatinib was schedule- and concentration-dependent and the sequential administration of honokiol before imatinib appeared to be more beneficial in K562 cells. Taken together, the data suggest that honokiol induced a novel cell death pathway and there was cross-talk between apoptotic and non-apoptotic programmed cell death caused by honokiol in leukemia cells. Moreover, honikiol exhibited schedule-dependent synergy in combination with imatinib and sequential administration of imatinib followed by honokiol could be the optimal sequence to combine these two drugs in K562 cells.

    Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzamides; Biphenyl Compounds; Cell Line, Tumor; Cell Membrane; Cell Proliferation; Drug Administration Schedule; Drug Synergism; Humans; Imatinib Mesylate; Leukemia; Lignans; Piperazines; Pyrimidines; Vacuoles

2010
Lignans from Santalum album and their cytotoxic activities.
    Chemical & pharmaceutical bulletin, 2010, Volume: 58, Issue:4

    A new neolignan, (7R,8R)-5-O-demethylbilagrewin (1), together with four known lignans (2-5), were isolated from the heartwood of Santalum album (Santalaceae). The structure of 1 was determined by analysis of extensive spectroscopic data. The isolated compounds and derivatives were evaluated for their cytotoxic activities against HL-60 human promyelocytic leukemia cells and A549 human lung adenocarcinoma cells. Compounds 1 and 2 exhibited cytotoxicity against HL-60 cells with IC(50) values of 1.5+/-0.02 and 4.3+/-0.13 microM, and against A549 cells with IC(50) values of 13.6+/-0.32 and 19.9+/-1.27 microM, respectively. The aldehyde group of 1 and 2 was revealed to be a structural requirement for the appearance of cytotoxicity in this type of lignans. These tumor cell deaths were shown to be mediated through induction of apoptosis.

    Topics: Adenocarcinoma; Antineoplastic Agents, Phytogenic; Apoptosis; Cell Line, Tumor; Cytotoxins; DNA Fragmentation; Humans; Leukemia; Lignans; Lung Neoplasms; Molecular Structure; Neoplasms; Santalum

2010
Natural antioxidants synergistically enhance the anticancer potential of AP9-cd, a novel lignan composition from Cedrus deodara in human leukemia HL-60 cells.
    Chemico-biological interactions, 2010, Dec-05, Volume: 188, Issue:3

    Antioxidants have been used as adjuvant with anticancer therapy to synergize the potential of the anti-neoplastic therapeutics. Based on the fact, we have studied the effect of three natural antioxidants curcumin, silymarin and acteoside on AP9-cd (standardized lignan composition from Cedrus deodara) induced cytotoxicity in human leukemia HL-60 cells. The antioxidant potential of individual test compounds was first evaluated with ferric reducing antioxidant power (FRAP) test, which revealed that all four molecules behave as antioxidants. The apoptotic potential of AP9-cd was significantly enhanced in HL-60 cells in the presence of curcumin, silymarin and acteoside. It was confirmed by using various models like MTT assay, DNA fragmentation, nuclei condensation, sub-Go DNA population, Annexin-V-FITC binding, ROS depletion and immunoblotting in HL-60 cells. AP9-cd and individual antioxidants alone at low doses (10μg and 10μM, respectively) have meager or no cytotoxicity in HL-60 cells, whereas in mutual combinations, there were 2-3 times enhancement in Annexin-V-FITC and sub-Go DNA population. Moreover, prominent DNA ladders were observed at low doses of AP9-cd in combinations with various antioxidants. The Hoechst staining of the nucleus also revealed the same results for the HL-60 cells treated with AP9-cd and different antioxidants. The molecular diagnostics revealed that the combinations induced a strong antioxidant effect which was correlated with the downregulation of NF-κB expression in the nucleus. Out of the three antioxidants, curcumin was found to be more potent than acteoside and silymarin in terms of enhancing the apoptotic potential of AP9-cd. These results propose an important role of natural antioxidant as adjuvant to enhance the anticancer potential of AP9-cd and more likely other anti-neoplastic therapeutics.

    Topics: Annexin A5; Antineoplastic Agents; Antioxidants; Apoptosis; Biological Products; Cedrus; Cell Cycle; Cell Proliferation; DNA Fragmentation; Down-Regulation; Drug Synergism; Ferric Compounds; Fluorescein-5-isothiocyanate; Fluoresceins; HL-60 Cells; Humans; Leukemia; Lignans; Membrane Potential, Mitochondrial; Necrosis; NF-kappa B; Nitric Oxide; Oxidation-Reduction; Reactive Oxygen Species

2010
Induction of G1 arrest and apoptosis by schisandrin C isolated from Schizandra chinensis Baill in human leukemia U937 cells.
    International journal of molecular medicine, 2009, Volume: 24, Issue:4

    We isolated two phytochemical lignans, schisandrin and schisandrin C, from Schizandra chinensis Baill and investigated their anti-cancer effects in human leukemia U937 cells. Schisandrin C inhibited cell growth in a dose-dependent manner, which was associated with the induction of G1 arrest of the cell cycle and apoptosis; schisandrin did not inhibit growth. Schisandrin C induced G1 arrest was correlated with down-regulation of cyclin D1, cyclin E, cyclin-dependent kinase (Cdk) 4 and E2Fs expression, inhibition of phosphorylation of retinoblastoma protein (pRB), and up-regulation of the Cdk inhibitor p21(WAF1/CIP1). In addition, schisandrin C-induced apoptosis was associated with down-regulation of expression of the anti-apoptotic proteins Bcl-2 and Bcl-xL, proteolytic activation of caspase-3 and -9, and a concomitant degradation of poly(ADP-ribose) polymerase (PARP). Furthermore, schisandrin C-induced apoptosis was significantly inhibited by a caspase-3 specific inhibitor z-DEVD-fmk, indicating an important role for caspase-3 in the schisandrin C mechanism. In summary, growth inhibition by schisandrin C is related to cell cycle arrest at G1 and induction of caspase-3-dependent apoptosis in U937 cells; these findings suggest that schisandrin C may be a useful chemotherapeutic agent.

    Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Cell Cycle; Cyclooctanes; DNA Fragmentation; G1 Phase; Humans; Leukemia; Lignans; Molecular Structure; Polycyclic Compounds; Schisandra; U937 Cells

2009
Induction of apoptosis in human leukemia cell (Jurkat) by neolignans isolated from seeds of Licaria puchury-major.
    Biological & pharmaceutical bulletin, 2009, Volume: 32, Issue:10

    Ethanol extract of the seeds of Licaria puchury-major, a Brazilian herbal medicine, was found to inhibit cell proliferation in human leukemia cell line (Jurkat) by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Bioassay-guided fractionation of the active components led to the isolation of one phenylpropanoid (1) and ten neolignans (2-11). The apoptosis-inducing activity of the compounds showing cytotoxicity in Jurkat cells was assessed by flow cytometric analysis. Among the identified neolignans, compounds 3, 4, 6 and 7 which have similar molecular structures, showed apoptotic activity. To elucidate the mechanism of apoptosis induction by neolignans, intracellular caspase-3, -8 and -9 activity in Jurkat cells was evaluated. Compound 4 markedly elevated the activity of caspase-3 and -9.

    Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Caspase 3; Caspase 8; Caspase 9; Cell Proliferation; Humans; Jurkat Cells; Lauraceae; Leukemia; Lignans; Molecular Structure; Phytotherapy; Plant Extracts; Propanols; Seeds

2009
A novel lignan composition from Cedrus deodara induces apoptosis and early nitric oxide generation in human leukemia Molt-4 and HL-60 cells.
    Nitric oxide : biology and chemistry, 2006, Volume: 14, Issue:1

    AP9-cd, a standardized lignan composition from Cedrus deodara consisting of (-)-wikstromal, (-)-matairesinol, and dibenzyl butyrolactol, showed cytotoxicity in several human cancer cell lines reported earlier. An attempt was made in this study to investigate the mechanism of cell death in human leukemia Molt-4 and HL-60 cells. It inhibited Molt-4 cell proliferation with 48-h IC(50) of approximately 15 microg/ml, increased sub-G0 cell fraction with no mitotic block, produced apoptotic bodies and induced DNA ladder formation. Flow cytometric analysis of annexinV-FITC/PI-stained cells showed time-related increase in apoptosis and post-apoptotic necrosis. All these biological end-points indicated cell death by apoptosis. Further, initial events involved massive nitric oxide (NO) formation within 4 h with subsequent late appearance of peroxides in cells; measured by flow cytometry using specific fluorescent probes. Persistently high levels of NO and peroxide appeared to decrease mitochondrial membrane potential (Psi(mt)) which was recovered by cyclosporin A in Molt-4 cells. AP9-cd caused 2-fold activation of caspase-3 in Molt-4 and 5-fold activation in HL-60 cells. Also caspases-8 and -9 were activated in HL-60 cells. Ascorbate suppressed the enhanced caspases activities indicating a pro-oxidant effect of AP9-cd. Further, caspase-3 activation correlated with NO generation that was partially impaired by nitric oxide synthase (NOS) inhibitors and ascorbate suggesting a role of pro-oxidant species in caspase-3 activation. AP9-cd produced no cytotoxicity in primary rat hepatocyte culture at the concentrations used. The studies indicated that AP9-cd mediated early NO formation leads to caspases activation, peroxide generation, and mitochondrial depolarization which may be responsible for mitochondrial-dependent and -independent apoptotic pathways involved in the killing of leukemia cells by AP9-cd.

    Topics: Animals; Apoptosis; Cedrus; Cell Division; Cell Line, Tumor; Cells, Cultured; Flow Cytometry; Hepatocytes; Humans; Leukemia; Lignans; Membrane Potentials; Necrosis; Nitric Oxide; Peroxides; Rats; Reactive Oxygen Species

2006
Compounds with DNA cleaving activity from Kadsura ananosma.
    Die Pharmazie, 2006, Volume: 61, Issue:10

    Two DNA cleavage agents, meso-dihydroguaiaretic acid (1) and isobavachalcone (2) together with the known alpha-ylangene, beta-sitosterol, daucosterol, pentacosane, hexacosanic acid and cerotic acid 1-monoglyceride were isolated from the stem barks of Kadsura ananosma Kerr for the first time. Compounds 1 and 2 showed relaxation of supercoiled DNA to nicked DNA. 1 represented a new structural type of DNA cleavage agent, while 2 was reported to show DNA strand-scission activity for the first time. 1 also showed significant cytotoxic effect on Hela and Leukemia cells in vitro.

    Topics: Cell Line, Tumor; Chalcones; DNA; DNA, Superhelical; Guaiacol; HeLa Cells; Humans; Kadsura; Leukemia; Lignans; Magnetic Resonance Spectroscopy; Mass Spectrometry; Nucleic Acid Conformation; Plant Bark; Plant Stems

2006
Cytotoxic coumarins and lignans from extracts of the northern prickly ash (Zanthoxylum americanum).
    Phytotherapy research : PTR, 2001, Volume: 15, Issue:5

    Four pyranocoumarins; dipetaline, alloxanthoxyletin, xanthoxyletin and xanthyletin; and two lignans; sesamin and asarinin were isolated from the northern prickly ash, Zanthoxylum americanum. To varying degrees, all inhibited the incorporation of tritiated thymidine into human leukaemia (HL-60) cells. Dipetaline was the most active with an IC(50) of 0.68 ppm, followed by alloxanthoxyletin (1.31 ppm), sesamin (2.71 ppm), asarinin (4.12 ppm), xanthoxyletin (3.48 ppm) and xanthylletin (3.84 ppm).

    Topics: Antineoplastic Agents; Coumarins; HL-60 Cells; Humans; Leukemia; Lignans; Plant Extracts; Plant Stems; Plants, Medicinal; Rosales

2001
1H-cyclopenta[b]benzofuran lignans from Aglaia species inhibit cell proliferation and alter cell cycle distribution in human monocytic leukemia cell lines.
    Zeitschrift fur Naturforschung. C, Journal of biosciences, 1999, Volume: 54, Issue:12

    Thirteen naturally occurring 1H-cyclopenta[b]benzofuran lignans of the rocaglamide type as well as one naturally occurring aglain congener all of them isolated from three Aglaia species (Aglaia duperreana, A. oligophylla and A. spectabilis) collected in Vietnam were studied for their antiproliferative effects using the human monocytic leukemia cell lines MONO-MAC-1 and MONO-MAC-6. Only rocaglamide type compounds showed significant inhibition of [3H-]thymidine incorporation and the most active compound didesmethylrocaglamide inhibited cell growth in a similar concentration range as the well-known anticancer drug vinblastine sulfate. Detailed structure-activity analysis indicated that the OH-group at C-8b which is a common structural feature of most naturally occurring rocaglamide compounds is essential for the described antiproliferative activity since replacement of this group by methylation led to a complete loss of the inhibitory activity for the resulting derivative. Rocaglamide derivatives rapidly inhibited DNA as well as protein biosynthesis of MONO-MAC-6 cells at concentrations well below those of actinomycin D or cycloheximide which were used as positive controls in the respective experiments. Didesmethylrocaglamide was furthermore able to induce growth arrest of MONO-MAC-1 cells in the G2/M and probably G0/G1-phase of the cell cycle with no morphological indication of cellular damage. Our data suggests that 1H-cyclopenta[b]benzofuran lignans of the rocaglamide type act primarily by a cytostatic mechanism.

    Topics: Antineoplastic Agents, Phytogenic; Benzofurans; Cell Cycle; Cell Division; Humans; Leukemia; Lignans; Plants; Tumor Cells, Cultured

1999
Leukaemia during podophyllotoxin treatment in a patient with juvenile chronic arthritis.
    Scandinavian journal of rheumatology, 1996, Volume: 25, Issue:5

    Topics: Acute Disease; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Juvenile; Glycosides; Humans; Leukemia; Lignans; Neoplasms, Second Primary; Podophyllotoxin

1996