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Natural products isolated from Tetragonula carbonaria cerumen modulate free radical-scavenging and 5-lipoxygenase activities in vitro.

Propolis and cerumen are plant-derived products found in honeybees and stingless bees, respectively. Although propolis is an ancient folk medicine, the bioactivities of cerumen obtained from Australian native stingless bees (Tetragonula carbonaria) have not been widely studied. Therefore, we investigated selected anti-oxidant and anti-inflammatory properties of T. carbonaria cerumen.

1516 related Products with: Natural products isolated from Tetragonula carbonaria cerumen modulate free radical-scavenging and 5-lipoxygenase activities in vitro.

Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon CELLKINES Natural Human I Anti 3 DG imidazolone Mon Cultrex In Vitro Angiogen Rat Anti-Mouse Interleuki Mouse Anti-Chicken Interl EZBlock™ Protease Inhib EZBlock™ Protease Inhib EZBlock™ Protease Inhib

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Sensitive detection and estimation of cell-derived peroxynitrite fluxes using fluorescein-boronate.

The specific and sensitive detection of peroxynitrite (ONOO/ONOOH) in biological systems is a great challenge due to its high reactivity towards several biomolecules. Herein, we validated the advantages of using fluorescein-boronate (Fl-B) as a highly sensitive fluorescent probe for the direct detection of peroxynitrite under biologically-relevant conditions in two different cell models. The synthesis of Fl-B was achieved by a very simply two-step conversion synthetic route with high purity (>99%) and overall yield (∼42%). Reactivity analysis of Fl-B with relevant biological oxidants including hydrogen peroxide (HO), hypochlorous acid (HOCl) and peroxynitrite were performed. The rate constant for the reaction of peroxynitrite with Fl-B was 1.7×10Ms, a million times faster than the rate constant measured for HO (k=1.7Ms) and 2,700 faster than HOCl (6.2×10Ms) at 37°C and pH 7.4. The reaction of Fl-B with peroxynitrite was significant even in the presence of physiological concentrations of CO, a well-known peroxynitrite reactant. Experimental and simulated kinetic analyses confirm that the main oxidation process of Fl-B takes place with peroxynitrite itself via a direct bimolecular reaction and not with peroxynitrite-derived radicals. Fl-B was successfully applied for the detection of endogenously-generated peroxynitrite by endothelial cells and in macrophage-phagocyted parasites. Moreover, the generated data allowed estimating the actual intracellular flux of peroxynitrite. For instance, ionomycin-stimulated endothelial cells generated peroxynitrite at a rate of ∼ 0.1μMs, while immunostimulated macrophages do so in the order of ∼1μMs inside T. cruzi-infected phagosomes. Fl-B revealed not to be toxic in concentrations up to 1mM for 24h. Cellular peroxynitrite detection was achieved by conventional laboratory fluorescence-based methods including flow cytometry and epi-fluorescence microscopy. Fl-B was shown to be more sensitive than the coumarin boronate due to a higher molar absorption coefficient and quantum yield. Overall, our results show that Fl-B is a kinetically selective and highly sensitive probe for the direct detection of cell-derived peroxynitrite.

2590 related Products with: Sensitive detection and estimation of cell-derived peroxynitrite fluxes using fluorescein-boronate.

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A novel mechanism for the pyruvate protection against zinc-induced cytotoxicity: mediation by the chelating effect of citrate and isocitrate.

Intracellular accumulation of free zinc contributes to neuronal death in brain injuries such as ischemia and epilepsy. Pyruvate, a glucose metabolite, has been shown to block zinc neurotoxicity. However, it is largely unknown how pyruvate shows such a selective and remarkable protective effect. In this study, we sought to find a plausible mechanism of pyruvate protection against zinc toxicity. Pyruvate almost completely blocked cortical neuronal death induced by zinc, yet showed no protective effects against death induced by calcium (ionomycin, NMDA) or ferrous iron. Of the TCA cycle intermediates, citrate, isocitrate, and to a lesser extent oxaloacetate, protected against zinc toxicity. We then noted with LC-MS/MS assay that exposure to pyruvate, and to a lesser degree oxaloacetate, increased levels of citrate and isocitrate, which are known zinc chelators. While pyruvate added only during zinc exposure did not reduce zinc toxicity, citrate and isocitrate added only during zinc exposure, as did extracellular zinc chelator CaEDTA, completely blocked it. Furthermore, addition of pyruvate after zinc exposure substantially reduced intracellular zinc levels. Our results suggest that the remarkable protective effect of pyruvate against zinc cytotoxicity may be mediated indirectly by the accumulation of intracellular citrate and isocitrate, which act as intracellular zinc chelators.

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TCP-1 theta antibody Sour BYL-719 Mechanisms: PI3K- AZD-3514 Mechanisms: Andr Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Thermal Shaker with cooli Rat Anti-CCT theta Antibo Rabbit Anti-Theophylline Sheep Anti-Theophylline 3 FDA Standard Frozen Tissu FDA Standard Frozen Tissu

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Electrochemical label-free degranulation monitoring for in-situ evaluation of cellular function.

We fabricated a degranulation monitoring device, combining ion-sensitive field-effect transistor (ISFET) and microperfusion system. The electrical properties of ISFET were maintained even after immobilization of RBL-2H3 mast cells on the sensor. We successfully demonstrated in-situ monitoring of degranulation from stimulated RBL-2H3 cells by ionomycin. Potential change was induced by the release of acid-granule contents, which result in local pH decrease on the sensor under physiological conditions. This microdevice is expected to contribute as a platform technology for evaluating induced immune responses by chemical compounds.

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MarkerGene™ LysoLive™ 5 L F-Solv 100% Formaldeh Cellufine Formyl , 50 ml Cellufine Formyl Media Cellufine Formyl , 500 ml Cellufine Formyl Media Cellufine Formyl Media Enzyme Label Diluent Enzyme Label Diluent Fraction V BSA powder, p Fraction V BSA powder, p Fraction V BSA powder, p

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Effects of polyphenols and lipids from Pennisetum glaucum grains on T-cell activation: modulation of Ca(2+) and ERK1/ERK2 signaling.

Pearl millet (PM), i.e., Pennisetum glaucum, is widely grown in Africa and known for its anti-oxidant and anti-hyperlipidemic properties.

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Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac 5α-N-Acetyl-2'H-androst-

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Development and validation of HTS assay for screening the calcium-activated chloride channel modulators in TMEM16A stably expressed CHO cells.

Calcium-activated chloride channels (CaCCs), for example TMEM16A, are widely expressed in a variety of tissues and are involved in many important physiological functions. We developed and validated an atomic absorption spectroscopy (AAS)-based detection system for high-throughput screening (HTS) of CaCC modulators. With this assay, Cl(-) flux from CHO cells stably transfected with TMEM16A is assayed indirectly, by measuring excess silver ions (Ag(+)) in the supernatant of AgCl precipitates. The screening process involved four steps: (1) TMEM16A CHO cells were incubated in high-K(+) and high-Cl(-) buffer with test compounds, and with ionomycin as Ca(2+) ionophore, for 12 min; (2) cells were washed with a low-K(+), Cl(-)-free and Ca(2+)-free buffer; (3) CaCC/TMEM16A were activated in high-K(+), Cl(-)-free buffer with ionomycin (10 μmol L(-1)) for 12 min; and (4) excess Ag(+) concentration was measured using an ion channel reader (ICR, an AAS system). The assay can be used to screen CaCC activators and inhibitors at the same time. With this assay, positive control drugs, including NPPB, CaCCinh-A01, flufenamic acid (Flu) and Eact, all had good concentration-dependent effects on CaCC/TMEM16A. NPPB and CaCCinh-A01 inhibited the CaCC/TMEM16A currents completely at 300 μmol L(-1), with IC50 values of 39.35 ± 4.72 μmol L(-1) and 6.35 ± 0.27 μmol L(-1), respectively; and Eact, activated CaCC/TMEM16A, with an EC50 value of 3.92 ± 0.87 μmol L(-1).

1955 related Products with: Development and validation of HTS assay for screening the calcium-activated chloride channel modulators in TMEM16A stably expressed CHO cells.

Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle GLP 1 ELISA Kit, Rat Gluc Glucose Assay With the La Screen Quest™ Colorimet Screen Quest™ Colorimet EnzyChrom™ Kinase Assay FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu

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Hypoxic preconditioning-induced mitochondrial protection is not disrupted in a cell model of mtDNA T8993G mutation-induced F1F0-ATP synthase defect: the role of mitochondrial permeability transition.

Transient opening of the mitochondrial permeability transition pore plays a crucial role in hypoxic preconditioning-induced protection. Recently, the cyclophilin-D component of the mitochondrial permeability transition pore has been shown to interact with and regulate the F1F0-ATP synthase. However, the precise role of the F1F0-ATP synthase and the interaction between cyclophilin-D and F1F0-ATP synthase in the mitochondrial permeability transition pore and hypoxic preconditioning remain uncertain. Here we found that a 1-h hypoxic preconditioning delayed apoptosis and improved cell survival after stimulation with various apoptotic inducers including H2O2, ionomycin, and arachidonic acid in mitochondrial DNA T8993G mutation (NARP) osteosarcoma 143B cybrids, an F1F0-ATP synthase defect cell model. This hypoxic preconditioning protected NARP cybrid cells against focal laser irradiation-induced oxidative stress by suppressing reactive oxygen species formation and preventing the depletion of cardiolipin. Furthermore, the protective functions of transient opening of the mitochondrial permeability transition pore in both NARP cybrids and wild-type 143B cells can be augmented by hypoxic preconditioning. Disruption of the interaction between cyclophilin-D and F1F0-ATP synthase by cyclosporin A attenuated the mitochondrial protection induced by hypoxic preconditioning in both NARP cybrids and wild-type 143B cells. Our results demonstrate that the interaction between cyclophilin-D and F1F0-ATP synthase is important in the hypoxic preconditioning-induced cell protection. This finding improves our understanding of the mechanism of mitochondrial permeability transition pore opening in cells in response to hypoxic preconditioning, and will be helpful in further developing new pharmacological agents targeting hypoxia-reoxygenation injury and mitochondria-mediated cell death.

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Turbo methanol extract inhibits bone resorption through regulation of T cell function.

Marine organisms have bioactive potential which has tremendous pharmaceutical promise. Emerging evidence highlights the importance of the interplay between bone and the immune system of which T lymphocytes and their product act as key regulators of bone resorption. In the present investigation we have analyzed the anti-osteoporotic effect of turbo methanol extract (TME) in the reversal of bone resoprtion. Forty-two female Swiss albino mice were used and randomly assigned into sham-operated group (sham) and six ovariectomized (OVX) subgroups, i.e. OVX with vehicle (OVX) that received daily oral administration of water ad libitum; OVX with estradiol (2mg/kg/day); and OVX with different doses of TME i.e. TME 100mg/kg, TME 50mg/kg, TME 25mg/kg and TME 12.5mg/kg. Oral administration of TME or estradiol started on the second week after ovariectomy for a period of 4weeks. We observed that the administration of TME increased the trabeculation in tibia and reduced the atrophy in the uterus. TME significantly decreased the serum alkaline phosphatase (ALP) and acid phosphatase (ACP) activity in OVX mice. Micro CT analysis revealed that the TME administration preserved the bone volume, connectivity density, trabecular number, trabecular thickness and trabecular separation in OVX mice. Bone mineralization was measured in different groups of mice by Raman spectroscopy. Reversal of bone resorption was observed in TME treated group of mice. To further investigate the mechanism of action of TME, we analyzed the T lymphocyte proliferation and profiles of cytokine TNFα and sRANKL in TME treated ovariectomized mice. Decrease in the elevation of T cell subsets was observed after the supplementation with TME. The extract significantly lowered the T cell proliferation responses to mitogens, phorbol 12-myristate 13-acetate (PMA) and ionomycin (Io) and phytohemagglutinin (PHA). A marked reduction in TNFα and sRANKL secretion in serum and TNFα in cell free supernatants of activated T lymphocytes was observed upon TME administration. TME could significantly inhibit the in vitro osteoclastogenesis and the bone resorption observed using artificial calcium coated slides. Collectively, these results indicate that TME has the potential to inhibit bone resorption and may prove to be a potential candidate for the development of an anti-osteoporosis drug.

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Self-adjuvanting influenza candidate vaccine presenting epitopes for cell-mediated immunity on a proteinaceous multivalent nanoplatform.

We exploit the features of a virus-like particle, adenoviral dodecahedron (Ad Dd), for engineering a multivalent vaccination platform carrying influenza epitopes for cell-mediated immunity. The delivery platform, Ad Dd, is a proteinaceous, polyvalent, and biodegradable nanoparticle endowed with remarkable endocytosis activity that can be engineered to carry 60 copies of a peptide. Influenza M1 is the most abundant influenza internal protein with the conserved primary structure. Two different M1 immunodominant epitopes were separately inserted in Dd external positions without destroying the particles' dodecahedric structure. Both kinds of DdFluM1 obtained through expression in baculovirus system were properly presented by human dendritic cells triggering efficient activation of antigen-specific T cells responses. Importantly, the candidate vaccine was able to induce cellular immunity in vivo in chickens. These results warrant further investigation of Dd as a platform for candidate vaccine, able to stimulate cellular immune responses.

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Multiple lung carcinoma ( MarkerGene™ LysoLive™ MOUSE ANTI BOVINE ROTAVIR Bone Morphogenetic Protei anti SLAM anti CDw150 IgG anti CD37 IgG2b (monoclon Growth Differentiation Fa Human Stromal Cell-Derive Human Beta-cell Attractin Amplite™ Fluorimetric F Mouse Anti-Influenza A Nu Mouse Anti-Influenza A He

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Effect of chloride channel inhibitors on cytosolic Ca2+ levels and Ca2+-activated K+ (Gardos) channel activity in human red blood cells.

DIDS, NPPB, tannic acid (TA) and AO1 are widely used inhibitors of Cl(-) channels. Some Cl(-) channel inhibitors (NPPB, DIDS, niflumic acid) were shown to affect phosphatidylserine (PS) scrambling and, thus, the life span of human red blood cells (hRBCs). Since a number of publications suggest Ca(2+) dependence of PS scrambling, we explored whether inhibitors of Cl(-) channels (DIDS, NPPB) or of Ca(2+)-activated Cl(-) channels (DIDS, NPPB, TA, AO1) modified intracellular free Ca(2+) concentration ([Ca(2+)]i) and activity of Ca(2+)-activated K(+) (Gardos) channel in hRBCs. According to Fluo-3 fluorescence in flow cytometry, a short treatment (15 min, +37 °C) with Cl(-) channels inhibitors decreased [Ca(2+)]i in the following order: TA > AO1 > DIDS > NPPB. According to forward scatter, the decrease of [Ca(2+)]i was accompanied by a slight but significant increase in cell volume following DIDS, NPPB and AO1 treatments. TA treatment resulted in cell shrinkage. According to whole-cell patch-clamp experiments, TA activated and NPPB and AO1 inhibited Gardos channels. The Cl(-) channel blockers further modified the alterations of [Ca(2+)]i following ATP depletion (glucose deprivation, iodoacetic acid, 6-inosine), oxidative stress (1 mM t-BHP) and treatment with Ca(2+) ionophore ionomycin (1 μM). The ability of the Cl(-) channel inhibitors to modulate PS scrambling did not correlate with their influence on [Ca(2+)]i as TA and AO1 had a particularly strong decreasing effect on [Ca(2+)]i but at the same time enhanced PS exposure. In conclusion, Cl(-) channel inhibitors affect Gardos channels, influence Ca(2+) homeostasis and induce PS exposure of hRBCs by Ca(2+)-independent mechanisms.

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Human Red Blood Cells Uni Rabbit Anti-Human Red Blo Macrophage Colony Stimula Macrophage Colony Stimula anti H inh human blood an voltage-dependent calcium Recombinant Human CA2 Pro Recombinant Human CA2 Pro Recombinant Human CA2 Pro Anti beta3 AR Human, Poly Screen Quest™ Colorimet Screen Quest™ Colorimet

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