stilbenes and sphingosine-1-phosphate

stilbenes has been researched along with sphingosine-1-phosphate* in 7 studies

Other Studies

7 other study(ies) available for stilbenes and sphingosine-1-phosphate

ArticleYear
Resveratrol exerts a biphasic effect on apolipoprotein M.
    British journal of pharmacology, 2016, Volume: 173, Issue:1

    Resveratrol exerts a range of beneficial actions in several areas of pathophysiology, including vascular biology. Here, we have investigated the effects of resveratrol on apolipoprotein M (apoM), a carrier and modulator of sphingosine 1-phosphate (S1P), a vasoactive lipid mediator.. We used a hepatoma cell line (HepG2), human primary hepatocytes and C57BL/6 mice. We measured apoM, S1P and related enzymes, LDL receptors and sirtuin1 activity, using Western blotting, RT-PCR and enzyme assays. We also used si-RNA to knock-down sirtuin1 in HepG2 cells.. In cultures of HepG2 cells, resveratrol (1-10 μM) increased intracellular apoM and S1P. High concentrations of resveratrol (100 μM) decreased extracellular (in the culture medium) apoM, whereas moderate concentrations of resveratrol (1-10 μM) increased extracellular apoM. High concentrations of resveratrol also increased LDL receptor expression, while all concentrations of resveratrol activated the histone deacetylase sirtuin1. In cultures of human primary hepatocytes, resveratrol, at all concentrations, increased both intra- and extracellular apoM. When wild-type mice were fed a resveratrol-containing chow (0.3% w/w) for 2 weeks, both the plasma and hepatic apoM and S1P levels were increased. However, the resveratrol diet did not affect hepatic LDL receptor levels in this in vivo study.. Resveratrol increased intra- and extracellular levels of apoM, along with intracellular S1P levels, while a high concentration of resveratrol reduced extracellular apoM. The present findings suggest that resveratrol has novel effects on the metabolic kinetics of S1P, a multi-functional bioactive phospholipid.

    Topics: Animals; Apolipoproteins; Apolipoproteins M; Dose-Response Relationship, Drug; Extracellular Space; Hep G2 Cells; Hepatocytes; Humans; Lipocalins; Lysophospholipids; Mice; Primary Cell Culture; Receptors, LDL; Resveratrol; RNA, Small Interfering; Sirtuin 1; Sphingosine; Stilbenes

2016
Polydatin attenuates AGEs-induced upregulation of fibronectin and ICAM-1 in rat glomerular mesangial cells and db/db diabetic mice kidneys by inhibiting the activation of the SphK1-S1P signaling pathway.
    Molecular and cellular endocrinology, 2016, May-15, Volume: 427

    We previously demonstrated that activation of sphingosine kinase 1 (SphK1)- sphingosine 1- phosphate (S1P) signaling pathway by high glucose (HG) plays a pivotal role in increasing the expression of fibronectin (FN), an important fibrotic component, by promoting the DNA-binding activity of transcription factor activator protein 1 (AP-1) in glomerular mesangial cells (GMCs) under diabetic conditions. As a multi-target anti-oxidative drug, polydatin (PD) has been shown to have renoprotective effects on experimental diabetes. However, whether PD could resist diabetic nephropathy (DN) by regulating SphK1-S1P signaling pathway needs further investigation. Here, we found that PD significantly reversed the upregulated FN and ICAM-1 expression in GMCs exposed to AGEs. Simultaneously, PD dose-dependently inhibited SphK1 levels at the protein expression and kinase activity and attenuated S1P production under AGEs treatment conditions. In addition, PD reduced SphK activity in GMCs transfected with wild-type SphK(WT) plasmid and significantly suppressed SphK1-mediated increase of FN and ICAM-1 levels under normal conditions. Furthermore, we found that the AGEs-induced upregulation of phosphorylation of c-Jun at Ser63 and Ser73 and c-Fos at Ser32, DNA-binding activity and transcriptional activity of AP-1 were blocked by PD. In comparison with db/db model group, PD treatment suppressed SphK1 levels (mRNA, protein expression, and activity) and S1P production, reversed the upregulation of FN, ICAM-1, c-Jun, and c-Fos in the kidney tissues of diabetic mice, and finally ameliorated renal injury in db/db mice. These findings suggested that the downregulation of SphK1-S1P signaling pathway is probably a novel mechanism by which PD suppressed AGEs-induced FN and ICAM-1 expression and improved renal dysfunction of diabetic models.

    Topics: Animals; Cells, Cultured; Diabetes Mellitus, Experimental; Drugs, Chinese Herbal; Female; Fibronectins; Glomerular Mesangium; Glucosides; Glycation End Products, Advanced; Humans; Hypoglycemic Agents; Intercellular Adhesion Molecule-1; Lysophospholipids; Male; Mice; Phosphotransferases (Alcohol Group Acceptor); Rats; Rats, Sprague-Dawley; Signal Transduction; Sphingosine; Stilbenes; Up-Regulation

2016
Resveratrol induces apoptosis of leukemia cell line K562 by modulation of sphingosine kinase-1 pathway.
    International journal of clinical and experimental pathology, 2015, Volume: 8, Issue:3

    To explore the effects of resveratrol in a human myelogenous leukemia cell line K562 and its potential molecular mechanisms. The anti-proliferation effect of resveratrol-induced apoptosis on K562 cells were detected using MTT assay. Western blotting was performed for detecting changes of SphK1 expression in total cell protein and membrane/cytosol protein in K562 cells respectively after exposure to resveratrol. A biochemical assay was used to measure the activity of SphK after treatment of resveratrol, and then S1P and ceramide levels were examined using ELISA kits. Hochest 33258 staining and flow cytometry were applied to detect the apoptosis condition of K562 cells treated with resveratrol. Resveratrol inhibited the proliferation and induced apoptosis in K562 cells in a dose and time-dependent manner. Western blotting revealed that resveratrol did not affect total SphK1 expression level in K562 cells, but significantly changed the translocation of SphK1, the membrane SphK1 was decreased while cytosol SphK1 level was elevated. The activity of SphK1 in resveratrol treated groups was decreased compared to control group with a significant decrease of S1P and increase of ceramide level. Furthermore, Hoechst 33258 staining and Annexin V-FITC analysis confirmed the notable apoptotic effect of resveratrol in its anti-leukemia process. Resveratrol-induced proliferation inhibition of K562 cells might be mediated through its modulation activity of SphK1 pathway by regulating S1P and ceramide levels, which then affected the proliferation and apoptosis process of leukemia cells. SphK1/S1P pathway represents a target of resveratrol in human leukemia.

    Topics: Annexin A5; Antineoplastic Agents; Apoptosis; Cell Membrane; Cell Proliferation; Ceramides; Cytosol; Dose-Response Relationship, Drug; Humans; K562 Cells; Leukemia, Myeloid; Lysophospholipids; Phosphotransferases (Alcohol Group Acceptor); Protein Transport; Resveratrol; Signal Transduction; Sphingosine; Stilbenes; Time Factors

2015
The expression of sphingosine-1 phosphate receptor-1 in chronic lymphocytic leukemia cells is impaired by tumor microenvironmental signals and enhanced by piceatannol and R406.
    Journal of immunology (Baltimore, Md. : 1950), 2014, Sep-15, Volume: 193, Issue:6

    Chronic lymphocytic leukemia (CLL) is characterized by the progressive accumulation of clonal B lymphocytes. Proliferation occurs in lymphoid tissues upon interaction of leukemic cells with a supportive microenvironment. Therefore, the mobilization of tissue-resident CLL cells into the circulation is a useful therapeutic strategy to minimize the reservoir of tumor cells within survival niches. Because the exit of normal lymphocytes from lymphoid tissues depends on the presence of sphingosine-1 phosphate (S1P) and the regulated expression of S1P receptor-1 (S1PR1), we investigated whether the expression and function of S1PR1 can be modulated by key microenvironment signals. We found that activation of CLL cells with CXCL12, fibroblast CD40L(+), BCR cross-linking, or autologous nurse-like cells reduces their S1PR1 expression and the migratory response toward S1P. Moreover, we found that S1PR1 expression was reduced in the proliferative/activated subset of leukemic cells compared with the quiescent subset from the same patient. Similarly, bone marrow-resident CLL cells expressing high levels of the activation marker CD38 showed a lower expression of S1PR1 compared with CD38(low) counterparts. Finally, given that treatment with BCR-associated kinase inhibitors induces a transient redistribution of leukemic cells from lymphoid tissues to circulation, we studied the effect of the Syk inhibitors piceatannol and R406 on S1PR1 expression and function. We found that they enhance S1PR1 expression in CLL cells and their migratory response toward S1P. Based on our results, we suggest that the regulated expression of S1PR1 might modulate the egress of the leukemic clone from lymphoid tissues.

    Topics: ADP-ribosyl Cyclase 1; Adult; Aged; Aged, 80 and over; Animals; B-Lymphocytes; CD40 Ligand; Cell Movement; Chemokine CXCL12; Female; Gene Expression; Gene Expression Regulation, Neoplastic; Humans; Intracellular Signaling Peptides and Proteins; Leukemia, Lymphocytic, Chronic, B-Cell; Lysophospholipids; Male; Membrane Glycoproteins; Mice; Middle Aged; Oxazines; Protein-Tyrosine Kinases; Proto-Oncogene Proteins c-bcr; Pyridines; Receptors, CXCR4; Receptors, Lysosphingolipid; Sphingosine; Sphingosine-1-Phosphate Receptors; Stilbenes; Syk Kinase; Tumor Cells, Cultured; Tumor Microenvironment

2014
Resveratrol stimulates sphingosine-1-phosphate signaling of cathelicidin production.
    The Journal of investigative dermatology, 2013, Volume: 133, Issue:8

    We recently discovered a regulatory mechanism that stimulates the production of the multifunctional antimicrobial peptide cathelicidin antimicrobial peptide (CAMP). In response to subtoxic levels of ER stress, increased sphingosine-1-phosphate (S1P) production activates an NFκBC/EBPα-dependent pathway that enhances CAMP production in cultured human keratinocytes. As the multifunctional stilbenoid compound resveratrol (RESV) increases ceramide (Cer) levels, a precursor of S1P, we hypothesized and assessed whether RESV could exploit the same pathway to regulate CAMP production. Accordingly, RESV significantly increased Cer and S1P levels in cultured keratinocytes, paralleled by increased CAMP mRNA/protein expression. Furthermore, topical RESV also increased murine CAMP mRNA/protein expression in mouse skin. Conversely, blockade of Cer-->sphingosine-->S1P metabolic conversion, with specific inhibitors of ceramidase or sphingosine kinase, attenuated the expected RESV-mediated increase in CAMP expression. The RESV-induced increase in CAMP expression required both NF-κB and C/EBPα transactivation. Moreover, conditioned media from keratinocytes treated with RESV significantly suppressed Staphylococcus aureus growth. Finally, topical RESV, if not coapplied with a specific inhibitor of sphingosine kinase, blocked S. aureus invasion into murine skin. These results demonstrate that the dietary stilbenoid RESV stimulates S1P signaling of CAMP production through an NF-κB-->C/EBPα-dependent mechanism, leading to enhanced antimicrobial defense against exogenous microbial pathogens.

    Topics: Animals; Antimicrobial Cationic Peptides; Antioxidants; Cathelicidins; CCAAT-Enhancer-Binding Protein-alpha; Cell Line, Transformed; Cyclic AMP; Endoplasmic Reticulum Stress; Epidermal Cells; Epidermis; Female; Humans; Immunity, Innate; Keratinocytes; Lysophospholipids; Mice; Mice, Hairless; NF-kappa B; Resveratrol; Signal Transduction; Sphingosine; Staphylococcal Skin Infections; Stilbenes

2013
Resveratrol triggers apoptosis through regulating ceramide metabolizing genes in human K562 chronic myeloid leukemia cells.
    Nutrition and cancer, 2011, Volume: 63, Issue:4

    Resveratrol, an important phytoalexin in many plants, has been reported to have cytotoxic effects on various types of cancer. Ceramide is a bioactive sphingolipid that regulates many signaling pathways, including cell growth and proliferation, senescence and quiescence, apoptosis, and cell cycle. Ceramides are generated by longevity assurance genes (LASS). Glucosylceramide synthase (GCS) and sphingosine kinase-1 (SK-1) enzymes can convert ceramides to antiapoptotic molecules, glucosylceramide, and sphingosine-1-phosphate, respectively. C8:ceramide, an important cell-permeable analogue of natural ceramides, increases intracellular ceramide levels significantly, while 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) and SK-1 inhibitor increase accumulation of ceramides by inhibiting GCS and SK-1, respectively. Chronic myelogenous leukemia (CML) is a hematological disorder resulting from generation of BCR/ABL oncogene. In this study, we examined the roles of ceramide metabolizing genes in resveratrol-induced apoptosis in K562 CML cells. There were synergistic cytotoxic and apoptotic effects of resveratrol with coadministration of C8:ceramide, PDMP, and SK-1 inhibitor. Interestingly, there were also significant increases in expression levels of LASS genes and decreases in expression levels of GCS and SK-1 in K562 cells in response to resveratrol. Our data, in total, showed for the first time that resveratrol might kill CML cells through increasing intracellular generation and accumulation of apoptotic ceramides.

    Topics: Apoptosis; Ceramides; Down-Regulation; Glucosylceramides; Glucosyltransferases; Humans; K562 Cells; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Lysophospholipids; Morpholines; Phosphotransferases (Alcohol Group Acceptor); Resveratrol; RNA, Neoplasm; Sphingosine; Stilbenes; Up-Regulation

2011
Inhibition of S1P by polyphenols prevents inflammation and angiogenesis: NFkappaB, a downstream effector?
    Free radical biology & medicine, 2007, Jan-15, Volume: 42, Issue:2

    Topics: Animals; Anti-Inflammatory Agents; Cell Movement; Flavonoids; Humans; Inflammation; Lysophospholipids; Neovascularization, Pathologic; NF-kappa B; Phenols; Polyphenols; Propiophenones; Resveratrol; Sphingosine; Stilbenes; Vitis

2007
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