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Berlin Brandenburg

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  • 1
    Language: English
    In: BMC Research Notes, June 23, 2014, Vol.7(1)
    Description: Background Different flavonoids are known to interfere with influenza A virus replication. Recently, we showed that the structurally similar flavonoids baicalein and biochanin A inhibit highly pathogenic avian H5N1 influenza A virus replication by different mechanisms in A549 lung cells. Here, we investigated the effects of both compounds on H5N1-induced reactive oxygen species (ROS) formation and the role of ROS formation during H5N1 replication. Findings Baicalein and biochanin A enhanced H5N1-induced ROS formation in A549 cells and primary human monocyte-derived macrophages. Suppression of ROS formation induced by baicalein and biochanin A using the antioxidant N-acetyl-L-cysteine strongly increased the anti-H5N1 activity of both compounds in A549 cells but not in macrophages. Conclusions These findings emphasise that flavonoids induce complex pharmacological actions some of which may interfere with H5N1 replication while others may support H5N1 replication. A more detailed understanding of these actions and the underlying structure-activity relationships is needed to design agents with optimised anti-H5N1 activity. Keywords: H5N1, Biochanin A, Baicalein, Antiviral, Reactive oxygen species, N-acetyl-L-cysteine
    Keywords: Antiviral Agents -- Research ; Antioxidants (Nutrients) -- Research ; Avian Influenza -- Research ; Cystine ; Avian Influenza Viruses ; Macrophages
    ISSN: 1756-0500
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  • 2
    Language: English
    In: PLoS ONE, Sept 30, 2014, Vol.9(9)
    Description: Aurora kinase inhibitors displayed activity in pre-clinical neuroblastoma models. Here, we studied the effects of the pan-aurora kinase inhibitor tozasertib (VX680, MK-0457) and the aurora kinase inhibitor alisertib (MLN8237) that shows some specificity for aurora kinase A over aurora kinase B in a panel of neuroblastoma cell lines with acquired drug resistance. Both compounds displayed anti-neuroblastoma activity in the nanomolar range. The anti-neuroblastoma mechanism included inhibition of aurora kinase signalling as indicated by decreased phosphorylation of the aurora kinase substrate histone H3, cell cycle inhibition in G2/M phase, and induction of apoptosis. The activity of alisertib but not of tozasertib was affected by ABCB1 expression. Aurora kinase inhibitors induced a p53 response and their activity was enhanced in combination with the MDM2 inhibitor and p53 activator nutlin-3 in p53 wild-type cells. In conclusion, aurora kinases are potential drug targets in therapy-refractory neuroblastoma, in particular for the vast majority of p53 wild-type cases.
    Keywords: Tumor Proteins ; Apoptosis ; Phosphotransferases ; Neuroblastoma
    ISSN: 1932-6203
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  • 3
    Language: English
    In: Molecular Cancer, 2009, Vol.8(1), pp.urn:issn:1476-4598
    Description: Background: Chemoresistance acquisition may influence cancer cell biology. Here, bioinformatics analysis of gene expression data was used to identify chemoresistance-associated changes in neuroblastoma biology. Results: Bioinformatics analysis of gene expression data revealed that expression of angiogenesis-associated...
    Keywords: Endothelial Growth-Factor ; In-Vivo ; Melanoma-Cells ; Tumor-Growth ; N-Myc ; Extracellular-Matrix ; Angiogenic Factors ; Cytokine Network ; Vegf Expression ; Blood-Vessels
    ISSN: 1476-4598
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  • 4
    Language: English
    In: PLoS ONE, May 17, 2011, Vol.6(5), p.e19705
    Description: Glycyrrhizin is known to exert antiviral and anti-inflammatory effects. Here, the effects of an approved parenteral glycyrrhizin preparation (Stronger Neo-Minophafen C) were investigated on highly pathogenic influenza A H5N1 virus replication, H5N1-induced apoptosis, and H5N1-induced pro-inflammatory responses in lung epithelial (A549) cells. Therapeutic glycyrrhizin concentrations substantially inhibited H5N1-induced expression of the pro-inflammatory molecules CXCL10, interleukin 6, CCL2, and CCL5 (effective glycyrrhizin concentrations 25 to 50 [micro]g/ml) but interfered with H5N1 replication and H5N1-induced apoptosis to a lesser extent (effective glycyrrhizin concentrations 100 [micro]g/ml or higher). Glycyrrhizin also diminished monocyte migration towards supernatants of H5N1-infected A549 cells. The mechanism by which glycyrrhizin interferes with H5N1 replication and H5N1-induced pro-inflammatory gene expression includes inhibition of H5N1-induced formation of reactive oxygen species and (in turn) reduced activation of NF[kappa]B, JNK, and p38, redox-sensitive signalling events known to be relevant for influenza A virus replication. Therefore, glycyrrhizin may complement the arsenal of potential drugs for the treatment of H5N1 disease.
    Keywords: Antiviral Agents -- Health Aspects ; Virus Replication -- Health Aspects ; Avian Influenza Viruses -- Health Aspects ; Avian Influenza -- Health Aspects ; Genes -- Health Aspects ; Apoptosis -- Health Aspects ; Gene Expression -- Health Aspects
    ISSN: 1932-6203
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  • 5
    Language: English
    In: Clinical Ophthalmology, Annual, 2013, Vol.7, p.1061(7)
    Description: Purpose: To assess the levels of inflammatory and angiogenic cytokines in undiluted vitreous from treatment-naive patients with macular edema secondary to nonischemic branch retinal vein occlusion (BRVO), with flow cytometric bead array (CBA) and to correlate the results with subjective and multiple spectral-domain optical coherence tomography (SD-OCT) parameters. Methods: A total of 43 eyes from 43 patients (mean age 69.7 years, 23 male) were divided into groups of new, "fresh" (n = 28; mean duration after onset 4.1 months) and older BRVO (n = 15; 11.6 months). Because of macular edema, these patients underwent an intravitreal therapy combining a single-site 23 g core vitrectomy with bevacizumab and dexamethasone. Undiluted vitreous was then analyzed for interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and vascular endothelial growth factor isoform A (VEGF-A) levels with CBA and correlated with visual acuity (VA), clinical parameters of BRVO (type and perfusion status), and morphologic parameters, such as central macular thickness, central retinal thickness, thickness of the neurosensory retina, thickness of the serous retinal detachment, and the disruption of the ellipsoid line (photoreceptor inner and outer segments) and the external limiting membrane, as measured with SD-OCT. Twenty-eight undiluted vitreous samples from patients with idiopathic, nonuveitis vitreous floaters served as the controls. Results: The mean IL-6 was 23.2 pg/mL (standard deviation, [+ or -]48.8), MCP-1 was 602.6 ([+ or -]490.3), and VEGF-A was 161.8 ([+ or -]314.3), and this was higher than in the control group, which had a mean IL-6 of 6.2 [+ or -] 3.4 pg/mL (P = 0.17), MCP-1 of 253.2 [+ or -] 73.5 (P 〈 0.0000001), and VEGF-A of 7.0 [+ or -] 4.9 (P 〈 0.003). In all BRVO samples, IL-6 correlated positively with MCP-1 and VEGF-A (correlation coefficient r = 0.79 and r = 0.46, respectively). VEGF-A was the only cytokine to correlate significantly with SD-OCT parameters (thickness of the neurosensory retina r = 0.31; disruption of the ellipsoid line r = 0.33). In the older BRVO group, there was a positive correlation between cytokines (IL-6 with MCP-1, r = 0.77; Il-6 with VEGF-A, r = 0.68; MCP-1 and VEGF-A, r = 0.68), whereas only IL-6 correlated with MCP-1 in the fresh group (r = 0.8). Conclusion: The inflammatory markers and VEGF-A were elevated in the vitreous fluid of patients with BRVO, and these correlated with one another. VEGF-A was more often correlated with the morphologic changes assessed by SD-OCT, whereas the inflammatory markers had no significant influence on SD-OCT changes. Keywords: vitreous samples, BRVO, VEGF, MCP, IL-6, CBA, SD-OCT
    Keywords: Cytokines -- Identification And Classification ; Body Fluids -- Composition ; Retinal Diseases -- Physiological Aspects ; Optical Tomography -- Methods
    ISSN: 1177-5483
    ISSN: 11775467
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  • 6
    Language: English
    In: Beilstein Journal of Nanotechnology, 01 August 2019, Vol.10(1), pp.1707-1715
    Description: Resistance to systemic drug therapy is a major reason for the failure of anticancer therapies. Here, we tested doxorubicin-loaded human serum albumin (HSA) nanoparticles in the neuroblastoma cell line UKF-NB-3 and its ABCB1-expressing sublines adapted to vincristine (UKF-NB-3rVCR1) and doxorubicin (UKF-NB-3rDOX20). Doxorubicin-loaded nanoparticles displayed increased anticancer activity in UKF-NB-3rVCR1 and UKF-NB-3rDOX20 cells relative to doxorubicin solution, but not in UKF-NB-3 cells. UKF-NB-3rVCR1 cells were re-sensitised by nanoparticle-encapsulated doxorubicin to the level of UKF-NB-3 cells. UKF-NB-3rDOX20 cells displayed a more pronounced resistance phenotype than UKF-NB-3rVCR1 cells and were not re-sensitised by doxorubicin-loaded nanoparticles to the level of parental cells. ABCB1 inhibition using zosuquidar resulted in similar effects like nanoparticle incorporation, indicating that doxorubicin-loaded nanoparticles successfully circumvent ABCB1-mediated drug efflux. The limited re-sensitisation of UKF-NB-3rDOX20 cells to doxorubicin by circumvention of ABCB1-mediated efflux is probably due to the presence of multiple doxorubicin resistance mechanisms. So far, ABCB1 inhibitors have failed in clinical trials probably because systemic ABCB1 inhibition results in a modified body distribution of its many substrates including drugs, xenobiotics, and other molecules. HSA nanoparticles may provide an alternative, more specific way to overcome transporter-mediated resistance.
    Keywords: Abcb1 ; Cancer ; Doxorubicin ; Drug Resistance ; Human Serum Albumin ; Nanoparticles ; Transporter ; Engineering
    ISSN: 2190-4286
    E-ISSN: 2190-4286
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