Light-controlled release of nitric oxide from solid polymer composite materials using visible and near infra-red light

2015 ◽  
Vol 14 (4) ◽  
pp. 775-785 ◽  
Author(s):  
Jonathan D. Mase ◽  
Anton O. Razgoniaev ◽  
Megan K. Tschirhart ◽  
Alexis D. Ostrowski

Composite materials were prepared using biocompatible polymers, upconverting nanoparticles, and a nitric oxide (NO) donor complex. We have demonstrated NO release from the solid composites after visible and near infra-red light irradiation.

2014 ◽  
Vol 2 (31) ◽  
pp. 5003-5011 ◽  
Author(s):  
Hien T. T. Duong ◽  
Nik Nik M. Adnan ◽  
Nicolas Barraud ◽  
Johan S. Basuki ◽  
Samuel K. Kutty ◽  
...  

Gold nanoparticles (size 10 nm) were designed to store and release nitric oxide (NO), by functionalizing their surfaces with functional polymers modified with NO-donor molecules.


2005 ◽  
Vol 390 (2) ◽  
pp. 625-631 ◽  
Author(s):  
Antonius C. F. Gorren ◽  
Michael Russwurm ◽  
Alexander Kollau ◽  
Doris Koesling ◽  
Kurt Schmidt ◽  
...  

GTN (nitroglycerin; glycerol trinitrate) causes dilation of blood vessels via activation of nitric oxide (NO)-sensitive sGC (soluble guanylate cyclase), a heterodimeric haem protein that catalyses the conversion of GTP into cGMP. Activation of sGC by GTN requires enzymatic or non-enzymatic bioactivation of the nitrate. Based on insufficient NO release and lack of spectroscopic evidence for formation of NO–sGC, the cysteine (Cys)-dependent activation of sGC by GTN was proposed to occur in an NO-independent manner. This extraordinary claim is questioned by the present findings. First, the effect of GTN/Cys was blocked by the NO scavenger oxyhaemoglobin, the superoxide-generating compound flavin mononucleotide and the haem-site sGC inhibitor ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one). Secondly, at equi-effective concentrations, GTN/Cys and the NO donor 2,2-diethyl-1-nitroso-oxyhydrazine released identical amounts of NO. Finally, at sufficiently high rates of NO release, activation of sGC by GTN/Cys was accompanied by a shift of the Soret band from 431 to 399 nm, indicating formation of NO–sGC. In the absence of Cys, GTN caused haem oxidation, apparent as a shift of the Soret band to 392 nm, which was accompanied by inactivation of the NO-stimulated enzyme. These results suggest that the effect of GTN/Cys is the result of an activation/inactivation equilibrium that is controlled by the rate of NO release and haem oxidation.


2000 ◽  
Vol 92 (6) ◽  
pp. 1677-1684 ◽  
Author(s):  
Ingeborg D. Welters ◽  
Axel Menzebach ◽  
Yannick Goumon ◽  
Patrick Cadet ◽  
Thilo Menges ◽  
...  

Background The transcription factor NF-kappaB plays a pivotal role in gene expression of inflammatory mediators such as cytokines or adhesion molecules. NF-kappaB-mediated transcriptional activation of these genes is inhibited by nitric oxide (NO) in a variety of cells, including monocytes. Morphine mediates NO release in a naloxone antagonizable manner in monocytes and neutrophils. Methods The influence of morphine on NF-kappaB activation was investigated in a whole-blood flow cytometric assay. A specific antibody against the p65 subunit of NF-kappaB was used and detected by fluoresceine-isothiocyanate-labeled anti-immunoglobulin G. Nuclei were stained with propidium iodide. Leukocyte subpopulations were evaluated by gating on neutrophils and monocytes. The median fluorescence channel was determined. Different morphine concentrations (50 nm, 50 microm, 1 mm) and incubation intervals (10-150 min) were used. Results Morphine inhibits lipopolysaccharide-induced NF-kappaB nuclear binding in human blood neutrophils and monocytes in a time-, concentration-, and naloxone-sensitive-dependent manner. Similar effects were achieved with the NO donor S-nitroso-N-acetyl-pencillamine and the antioxidant N-acetyl-cysteine. The NO synthase inhibitors Nomega-nitro-l-arginine-methyl-esther and Nomega-nitro-l-arginine completely abolished the morphine-induced attenuation of NF-kappaB nuclear binding, demonstrating that the inhibitory action is mediated by NO release. Conclusion Morphine causes immunosuppression, at least in part, via the NO-stimulated depression of NF-kappaB nuclear binding.


2017 ◽  
Vol 15 (13) ◽  
pp. 2791-2796 ◽  
Author(s):  
Hana Okuno ◽  
Naoya Ieda ◽  
Yuji Hotta ◽  
Mitsuyasu Kawaguchi ◽  
Kazunori Kimura ◽  
...  

A novel yellowish-green-light-controllable NO donor, NO-Rosa, was synthesized. With NO-Rosa, NO release in cells and NO-induced vasodilation were photocontrolled.


2011 ◽  
Vol 236-238 ◽  
pp. 2967-2972 ◽  
Author(s):  
Yong Liu ◽  
Yan Sun ◽  
Peng Yang ◽  
Yao Xing Xu ◽  
Yan Li Li ◽  
...  

This work aims to prepare and characterize one kind of nitric oxide (NO)-releasing conjugation of quaternary ammonium salt to chitosan, as well as to evaluate the anti-bacterial properties of diazeniumdiolates and the changes in NO release properties. The newly synthesized diazeniumdiolates are obtained from glycidyl-trimethyl-ammonium chloride (GTMAC)-bearing chitosan derivatives (HTCC) with different molecular weights (280 and 670 KDa) and are used as NO donor species. An HTCC with high molecular weight (670 KDa) exhibits higher storage capacity for NO (up to 357.70 nmol NO/mg) than one with a low molecular weight (280 kDa). The NO release durations (7 h) observed for the HTCC diazeniumliolates with higher molecular weight (670 kDa) was slightly higher than that of HTCC diazeniumliolates with lower molecular weight (280 kDa). By determining the inhibition zone diameter, HTCC-NO with lower molecular weight (280 kDa) showed significantly higher inhibition capabilities againstE. colithan HTCC, crude chitosan, and water control.


Author(s):  
Giovanna Jardim Vieira P. dos Santos ◽  
Marcelo Ganzarolli de Oliveira ◽  
Guilherme Fadel Picheth ◽  
Valéria Póvoa ◽  
Eliana Pereira de Araujo

Nitric oxide (NO) donor biomaterials have great potential to promote tissue regeneration and healing. Among the materials that can be used for this purpose, collagen has high biocompatibility, low antigenic activity and is already used commercially in the form of membranes with hemostatic action for the coating of lesions to favor the regeneration of the injured area. NO is directly involved in angiogenic and proliferative activities, stimulating the tissue repair process in healthy individuals or patients suffering from chronic diseases (e.g. diabetes). The collagen membranes were impregnated with S-nitrosoglutathione (GSNO), a NO donor, through absorption from solution and characterized by vibrational spectroscopy, scanning electron microscopy and dispersive energy spectroscopy. NO release was characterized by chemiluminescence. The kinetics of NO release were shown to be dependent on the hydration degree. In vivo experiments showed that collagen/GSNO membranes accelerate wound healing and increase the expression of cytokines associated with cell proliferation in cicatricial tissue of animals compared with control animals. These results show collagen/GSNO membranes exert an effective wound healing action and have potential to treat chronic ulcers.


Author(s):  
Sergii A. Sergiienko ◽  
David M. Tobaldi ◽  
Luc Lajaunie ◽  
Daniela V. Lopes ◽  
Gabriel Constantinescu ◽  
...  

The TiO2/MXene composites prepared by different routes were assessed towards the degradation of organic pollutants under simulated solar light. A notable photocatalytic activity of bare MXene under near infra-red light was discovered.


1996 ◽  
Vol 270 (3) ◽  
pp. C794-C802 ◽  
Author(s):  
E. Noiri ◽  
T. Peresleni ◽  
N. Srivastava ◽  
P. Weber ◽  
W. F. Bahou ◽  
...  

The restitution of epithelial integrity is accomplished in part by cell migration. Studying this process, we have found that nitric oxide (NO) release migrating epithelial BSC-1 cells displayed a biphasic response to the inflicted wounds; an initial transient release of NO is followed by a delayed sustained elevation. Whereas the constitutive endothelial NO synthase (NOS) did not show any spatial or temporal changes associated with wounding, the inducible NOS became expressed 3 h after wounding and showed higher abundance at the edges of epithelial wounds. L-Arginine (L-Arg) or NO donor, S-nitroso-N-acetyl-DL-penicillamine, exerted motogenic effect in epithelial and endothelial cells. Inhibition of NOS with NG-nitro-L-arginine methyl ester (L-NAME) or a selective knockout of inducible NOS with antisense oligodeoxynucleotides reduced the rate of spontaneous or epidermal growth factor (EGF)-induced BSC-1 cell migration. Migrating cells showed the polarized expression of NOS, suggesting a head-to-rear NO gradient. Several growth factors (EGF, insulin-like growth factor I, hepatocyte growth factor, and fibroblast growth factor) were motogenic for BSC-1 cells, but this effect was abrogated by pretreatment with L-NAME. We conclude that endogenous NO production is a prerequisite for BSC-1 cell migration. A vectorial NO release may be essential for the spatially and temporally coordinated reciprocal phenomena that occur at the leading and trailing edge of locomoting epithelial cells. Although the exact mode of NO action remains uncertain, it is conceivable that the production of NO serves as a cellular switch from the stationary to the locomoting epithelial phenotype.


2016 ◽  
Vol 4 (11) ◽  
pp. 1987-1998 ◽  
Author(s):  
Alec Lutzke ◽  
Bella H. Neufeld ◽  
Megan J. Neufeld ◽  
Melissa M. Reynolds

First report of nitric oxide (NO) release from a biodegradable polyphosphazene containing theS-nitrosothiol NO donor group.


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