scholarly journals Rosmarinic Acid-Rich Extracts of Summer Savory (Satureja hortensisL.) Protect Jurkat T Cells against Oxidative Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Irakli Chkhikvishvili ◽  
Tamar Sanikidze ◽  
Nunu Gogia ◽  
Tamar Mchedlishvili ◽  
Maia Enukidze ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Rosmarinic Acid ◽  
Jurkat Cells ◽  
Peroxyl Radicals ◽  
G1 Arrest ◽  
Acid Fraction ◽  
Cellular Mechanisms ◽  
Jurkat T Cells ◽  
Phenolic Fraction

Summer savory (Satureja hortensisL.,Lamiaceae) is used in several regions of the world as a spice and folk medicine. Anti-inflammatory and cytoprotective effects ofS. hortensisand of its rosmarinic acid-rich phenolic fraction have been demonstrated in animal trials. However, previous studies of rosmarinic acid in cell models have yielded controversial results. In this study, we investigated the effects of summer savory extracts on H2O2-challenged human lymphoblastoid Jurkat T cells. LC-MS analysis confirmed the presence of rosmarinic acid and flavonoids such as hesperidin and naringin in the phenolic fraction. Adding 25 or 50 µM of H2O2to the cell culture caused oxidative stress, manifested as generation of superoxide and peroxyl radicals, reduced cell viability, G0/G1 arrest, and enhanced apoptosis. This stress was significantly alleviated by the ethanolic and aqueous extracts ofS. hortensisand by the partially purified rosmarinic acid fraction. The application of an aqueousS. hortensisextract doubled the activity of catalase and superoxide dismutase in the cells. The production of IL-2 and IL-10 interleukins was stimulated by H2O2and was further enhanced by the addition of theS. hortensisextract or rosmarinic acid fraction. The H2O2-challenged Jurkat cells may serve as a model for investigating cellular mechanisms of cytoprotective phytonutrient effects.

scholarly journals Constituents of French Marigold (Tagetes patulaL.) Flowers Protect Jurkat T-Cells against Oxidative Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Irakli Chkhikvishvili ◽  
Tamar Sanikidze ◽  
Nunu Gogia ◽  
Maia Enukidze ◽  
Marine Machavariani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
T Cells ◽  
Radical Scavenging ◽  
Jurkat Cells ◽  
Cellular Mechanisms ◽  
Jurkat T Cells ◽  
Radical Scavenging Capacity ◽  
Scavenging Capacity ◽  
Anti Inflammatory

The flowers of French marigold (Tagetes patulaL.) are widely used in folk medicine, in particular for treating inflammation-related disorders. However, cellular mechanisms of this activity demand further investigation. In the present work, we studied the potential ofT. patulacompounds to alleviate the oxidative stress in hydrogen peroxide-challenged human lymphoblastoid Jurkat T-cells. Crude extracts of marigold flowers and purified fractions containing flavonoids patuletin, quercetagetin, and quercetin and their derivatives, as well as the carotenoid lutein, were brought in contact with Jurkat cells challenged with 25 or 50 μM H2O2. Hydrogen peroxide caused oxidative stress in the cells, manifested as generation of superoxide and peroxyl radicals, reduced viability, arrested cell cycle, and enhanced apoptosis. The stress was alleviated by marigold ingredients that demonstrated high radical-scavenging capacity and enhanced the activity of antioxidant enzymes involved in neutralization of reactive oxygen species. Flavonoid fraction rich in quercetin and quercetagetin showed the highest cytoprotective activity, while patuletin in high dose exerted a cytotoxic effect associated with its anticancer potential.T. patulacompounds enhanced the production of anti-inflammatory and antioxidant interleukin-10 (IL-10) in Jurkat cells. Both direct radical-scavenging capacity and stimulation of protective cellular mechanisms can underlay the anti-inflammatory properties of marigold flowers.

scholarly journals Stimulation of CD28 triggers an association between CD28 and phosphatidylinositol 3-kinase in Jurkat T cells.

1994 ◽  
Vol 179 (3) ◽  
pp. 1071-1076 ◽  
Author(s):  
K E Truitt ◽  
C M Hicks ◽  
J B Imboden
Keyword(s):  
T Cells ◽  
Growth Factor Receptor ◽  
Jurkat Cells ◽  
Phosphatidylinositol 3 Kinase ◽  
Jurkat T Cells ◽  
Cell Surface Molecule ◽  
Natural Ligand ◽  
High Affinity Binding Site ◽  
Stimulation Of ◽  
Phosphatidylinositol 3

The T cell surface molecule CD28 can provide costimulatory signals that permit the full activation of T cells. Here we demonstrate that stimulation of CD28, either by B7, its natural ligand, or by the anti-CD28 monoclonal antibody 9.3, induces an association between CD28 and phosphatidylinositol 3-kinase (PI3-K) in Jurkat T cells, raising the possibility that an interaction with PI3-K contributes to CD28-mediated signaling. To examine the mechanism of the association, we synthesized tyrosine-phosphorylated oligopeptides corresponding to each of the four tyrosines in the CD28 cytoplasmic domain. When added to lysates of B7-stimulated Jurkat cells, the oligopeptide corresponding to Tyr 173 inhibits the coimmunoprecipitation of PI3-K with CD28; the other oligopeptides have no effect. Tyr 173 is contained within the sequence YMNM, a motif that is also found in the platelet-derived growth factor receptor and that, when phosphorylated, forms a high affinity binding site for the p85 subunit of PI3-K. These observations suggest that phosphorylation of Tyr 173 may mediate the interaction between CD28 and PI3-K. However, because CD28 is not known to be phosphorylated, it remains possible that CD28 interacts with PI3-K through a mechanism independent of tyrosine phosphorylation.

scholarly journals Interactions of Cbl with Grb2 and phosphatidylinositol 3'-kinase in activated Jurkat cells.

1995 ◽  
Vol 15 (7) ◽  
pp. 3571-3578 ◽  
Author(s):  
H Meisner ◽  
B R Conway ◽  
D Hartley ◽  
M P Czech
Keyword(s):  
T Cells ◽  
Kinase Activity ◽  
Cell Receptor ◽  
Sh2 Domain ◽  
Jurkat Cells ◽  
Cross Linking ◽  
Jurkat T Cells ◽  
Son Of Sevenless ◽  
Src Homology ◽  
Tcr Activation

T-cell receptor (TCR) cross-linking increases tyrosine phosphorylation of multiple proteins, only a few of which have been identified. One of the most rapidly tyrosine-phosphorylated polypeptides is the 120-kDa product of the proto-oncogene c-cbl, a cytosolic and cytoskeletal protein containing multiple proline-rich motifs that are potential binding sites for proteins containing Src homology 3 (SH3) domains. We report here that in cultured Jurkat T cells, Cbl is coprecipitated with antibody against the adapter protein Grb2. Upon activation of Jurkat T cells via the TCR-CD3 complex, we find that high-affinity binding of Cbl requires the N-terminal SH3 domain of GST-Grb2 fusion protein but after cross-linking of the TCR-CD3 and CD4 receptors, Cbl binds equally to its SH2 domain. Grb2 antisera also precipitated p85 from serum-starved cells, while TCR activation increased p85 and tyrosine-phosphorylated Cbl but not Cbl protein in Grb2 immunocomplexes. Phosphatidylinositol (PI) 3-kinase activity was immunoprecipitated from serum-starved cells with Cbl and to a lesser extent with Grb2 antisera, and TCR cross-linking increased this activity severalfold. The PI 3-kinase activity associated with Cbl amounted to 5 to 10% of the total cellular activity that could be precipitated by p85 antisera. The Ras exchange factor Son-of-sevenless 1 (Sos-1) was not found in anti-Cbl immunoprecipitates from activated cells, and Cbl was not detectable in anti-Sos-1 precipitates, supporting the likelihood that Sos-Grb2 and Cbl-Grb2 are present as distinct complexes. Taken together, these data suggest that Cbl function in Jurkat T cells involves its constitutive association with Grb2 and its recruitment of PI 3-kinase in response to TCR activation.

scholarly journals Antiproliferative Activity of the Isofuranonaphthoquinone Isolated fromBulbine frutescensagainst Jurkat T Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Penelope Tambama ◽  
Berhanu Abegaz ◽  
Stanley Mukanganyama
Keyword(s):  
T Cells ◽  
Anticancer Drug ◽  
Glutathione Transferase ◽  
Reduced Glutathione ◽  
Synergistic Effects ◽  
Drug Efflux ◽  
Cellular Mechanisms ◽  
Jurkat T Cells ◽  
Public Health Burden ◽  
Drug Efflux Pumps

Cancer is a major public health burden in both developed and developing countries. The quinone moiety has been shown to possess antitumor activity and several cancer drugs in clinical use contain this entity. The effect of isofuranonaphthoquinone isolated fromBulbine frutescenson Jurkat T cells was determined. Cells were exposed to the isofuranonaphthoquinone (IFNQ) at different concentrations. Significant antiproliferative effects were observed which were comparable to that of the anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). A combination of IFNQ with BCNU produced synergistic effects which were observed after 72 hrs. It was also observed that combining IFNQ with reduced glutathione abolished the anticancer activity of the compound. It is, therefore, proposed that the isofuranonaphthoquinone may exert part of its effect by producing reactive oxygen species resulting in death of the cells as the effects of this compound were antagonized by reduced glutathione. An investigation on the effects of isofuranonaphthoquinone on glutathione transferase (GST) activity and drug efflux pumps showed that this compound exhibited inhibitory effects on both the GST and the drug efflux pumping activities. Thus, the isofuranonaphthoquinone showed cytotoxicity, works through inhibition of some cellular mechanisms, and could present a potential source of lead compounds for anticancer drug development.

scholarly journals Titanium Ions Promote Exogenous Calcium-Dependent Calcium Influx in Activated Jurkat T Cells: A Possible Mechanism to Explain Its Immunostimulatory Properties

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Jing Chen ◽  
Qiuying Li ◽  
Zhenhua Pang ◽  
Ming Gong ◽  
Li Tang
Keyword(s):  
T Cells ◽  
T Cell ◽  
Intracellular Calcium ◽  
T Cell Activation ◽  
Calcium Influx ◽  
Biological Activities ◽  
Jurkat Cells ◽  
Dependent Manner ◽  
Jurkat T Cells ◽  
Exogenous Calcium

Titanium and its alloys have been widely used in dental and orthopedic implants. Owing to the biotribocorrosion behavior of implants in simulated oral environment, Ti(IV) ions could be released into surrounding tissues. Current studies have found that Ti(IV) ions could affect the biological activities of immune cells in adjacent tissues and subsequently jeopardize the long-term performance of implant prostheses. However, the potential mechanism underlying its immunomodulatory properties remains unclear. Calcium signaling has been confirmed to be involved in regulation of lymphocyte immune function. Therefore, we hypothesize that Ti(IV) ions modulated T cell function through the change of intracellular calcium concentrations. This study is aimed at exploring the role of intracellular calcium responses in the modulatory effect of Ti(IV) ions on unactivated and phytohemagglutinin-activated Jurkat T cells. Here, we confirmed that Ti(IV) ions within a certain concentration range induced CD69 expression on both unactivated and activated T cells in our study. Additionally, the combined stimulation with Ti(IV) ions and PHA increased expression of IL-1β, TNF-α, and RANKL. Furthermore, we found that treatment with Ti(IV) induced a transitory increase in the levels of [Ca2+]i in activated Jurkat cells, dependent on the presence of exogenous calcium. Treatment with different doses of Ti(IV) for 24 h significantly increased the levels of [Ca2+]i in the activated Jurkat cells in a dose-dependent manner, but had little effect in the unactivated cells. Treatment with Ti(IV) did not significantly affect the PLCγ1 activation and inositol-1,4,5-trisphosphate (IP3) secretion in Jurkat cells. Taken together, these data indicated that Ti(IV) enhanced calcium influx during the T cell activation, independent of IP3-mediated intracellular calcium release. Our work provides insights into the mechanism involved in the regulation of lymphocyte behaviors under the effect of Ti(IV) ions, which may help to develop therapeutic strategies for dental implant failures.

scholarly journals ZAP-70-Independent Ca2+ Mobilization and Erk Activation in Jurkat T Cells in Response to T-Cell Antigen Receptor Ligation

2001 ◽  
Vol 21 (21) ◽  
pp. 7137-7149 ◽  
Author(s):  
Xiaochuan Shan ◽  
Richard Balakir ◽  
Gabriel Criado ◽  
Jason S. Wood ◽  
Maria-Cristina Seminario ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Tyrosine Phosphorylation ◽  
Antigen Receptor ◽  
Jurkat Cells ◽  
Jurkat T Cells ◽  
T Cell Antigen Receptor ◽  
Erk Activation ◽  
Cell Antigen Receptor ◽  
Cell Antigen

ABSTRACT The tyrosine kinase ZAP-70 has been implicated as a critical intermediary between T-cell antigen receptor (TCR) stimulation and Erk activation on the basis of the ability of dominant negative ZAP-70 to inhibit TCR-stimulated Erk activation, and the reported inability of anti-CD3 antibodies to activate Erk in ZAP-70-negative Jurkat cells. However, Erk is activated in T cells receiving a partial agonist signal, despite failing to activate ZAP-70. This discrepancy led us to reanalyze the ZAP-70-negative Jurkat T-cell line P116 for its ability to support Erk activation in response to TCR/CD3 stimulation. Erk was activated by CD3 cross-linking in P116 cells. However, this response required a higher concentration of anti-CD3 antibody and was delayed and transient compared to that in Jurkat T cells. Activation of Raf-1 and MEK-1 was coincident with Erk activation. Remarkably, the time course of Ras activation was comparable in the two cell lines, despite proceeding in the absence of LAT tyrosine phosphorylation in the P116 cells. CD3 stimulation of P116 cells also induced tyrosine phosphorylation of phospholipase C-γ1 (PLCγ1) and increased the intracellular Ca2+ concentration. Protein kinase C (PKC) inhibitors blocked CD3-stimulated Erk activation in P116 cells, while parental Jurkat cells were refractory to PKC inhibition. The physiologic relevance of these signaling events is further supported by the finding of PLCγ1 tyrosine phosphorylation, Erk activation, and CD69 upregulation in P116 cells on stimulation with superantigen and antigen-presenting cells. These results demonstrate the existence of two pathways leading to TCR-stimulated Erk activation in Jurkat T cells: a ZAP-70-independent pathway requiring PKC and a ZAP-70-dependent pathway that is PKC independent.

Vitamin E synthetic derivate—TPGS—selectively induces apoptosis in jurkat t cells via oxidative stress signaling pathways: implications for acute lymphoblastic leukemia

APOPTOSIS ◽  
2016 ◽  
Vol 21 (9) ◽  
pp. 1019-1032 ◽  
Author(s):  
Cristian Ruiz-Moreno ◽  
Marlene Jimenez-Del-Rio ◽  
Ligia Sierra-Garcia ◽  
Betty Lopez-Osorio ◽  
Carlos Velez-Pardo
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Vitamin E ◽  
Acute Lymphoblastic Leukemia ◽  
Signaling Pathways ◽  
Lymphoblastic Leukemia ◽  
Stress Signaling ◽  
Jurkat T Cells

scholarly journals HIV-1 tat expression and sulphamethoxazole hydroxylamine mediated oxidative stress alter the disulfide proteome in Jurkat T cells

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Kemi Adeyanju ◽  
John R. Bend ◽  
Michael J. Rieder ◽  
Gregory A. Dekaban
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Jurkat T Cells ◽  
Hiv 1
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