Correlating S-nitrosothiol decomposition and NO release for modified poly(lactic-co-glycolic acid) polymer films

RSC Advances ◽  
2014 ◽  
Vol 4 (79) ◽  
pp. 42039-42043 ◽  
Author(s):  
J. M. Joslin ◽  
B. H. Neufeld ◽  
Melissa M. Reynolds

The decomposition of an S-nitrosated model polymer was correlated to the subsequent release of nitric oxide under multiple decomposition pathways.

2017 ◽  
Vol 8 ◽  
pp. 1637-1641
Author(s):  
Kathleen Lange ◽  
Christian Lautenschläger ◽  
Maria Wallert ◽  
Stefan Lorkowski ◽  
Andreas Stallmach ◽  
...  

We here describe a new approach to visualise nitric oxide (NO) in living macrophages by fluorescent NO-sensitive microspheres based on poly(lactic-co-glycolic acid) (PLGA). PLGA microspheres loaded with NO550 dye were prepared through a modified solvent-evaporation method. Microparticles were characterized by a mean hydrodynamic diameter of 3000 nm, zeta potential of −26.000 ± 0.351 mV and a PDI of 0.828 ± 0.298. Under abiotic conditions, NO release was triggered through UV radiation (254 nm) of 10 mM sodium nitroprusside dehydrate (SNP). After incubation, AZO550 microspheres exhibited an about 8-fold increased emission at 550 nm compared to NO550 particles. For biotic NO release, RAW 264.7 murine macrophages were activated with lipopolysaccharide (LPS) of Salmonella typhimurium. After treatment with NO550 microparticles, only activated cells caused a green particle fluorescence and could be detected by laser scanning microscopy. NO release was confirmed indirectly with Griess reaction. Our functional NO550 particles enable a simple and early evaluation of inflammatory and immunological processes. Furthermore, our results on particle-based NO sensing and previous studies in targeting intestinal inflammation via (PLGA)-based microspheres demonstrate that an advanced concept for visualizing intestinal inflammation is tangible.


2017 ◽  
Vol 5 (7) ◽  
pp. 1265-1278 ◽  
Author(s):  
Yaqi Wo ◽  
Li-Chong Xu ◽  
Zi Li ◽  
Adam J. Matzger ◽  
Mark E. Meyerhoff ◽  
...  

SNAP-impregnated textured polymer films having up to 38 day NO-release were shown to have synergistic effects in inhibiting bacterial adhesion.


2020 ◽  
Vol 21 (12) ◽  
pp. 4972-4979
Author(s):  
Yoogyeong Oh ◽  
Hyejoong Jeong ◽  
Sungmin Lim ◽  
Jinkee Hong

1994 ◽  
Vol 267 (1) ◽  
pp. F190-F195 ◽  
Author(s):  
H. Tsukahara ◽  
Y. Krivenko ◽  
L. C. Moore ◽  
M. S. Goligorsky

It has been hypothesized that fluctuations of the ionic composition in the interstitium of juxtaglomerular apparatus (JGA) modulate the function of extraglomerular mesangial cells (MC), thereby participating in tubuloglomerular feedback (TGF) signal transmission. We examined the effects of isosmotic reductions in ambient sodium concentration ([Na+]) and [Cl-] on cytosolic calcium concentration ([Ca2+]i) in cultured rat MC. Rapid reduction of [Na+] or [Cl-] in the bath induced a concentration-dependent rise in [Ca2+]i. MC are much more sensitive to decreases in ambient [Cl-] than to [Na+]; a decrease in [Cl-] as small as 14 mM was sufficient to elicit a detectable [Ca2]i response. These observations suggest that MC can be readily stimulated by modest perturbations of extracellular [Cl-]. Next, we examined whether activation of MC by lowered ambient [Cl-] influences cellular nitric oxide (NO) production. Using an amperometric NO sensor, we found that a 13 mM decrease in ambient [Cl-] caused a rapid, Ca2+/calmodulin-dependent rise in NO release from MC. This response was not inhibitable by dexamethasone, indicating the involvement of the constitutive rather than the inducible type of NO synthase in MC. In addition, the NO release was blunted by indomethacin pretreatment, suggesting that a metabolite(s) of cyclooxygenase regulates the activation of NO synthase in MC. Our findings that small perturbations in external [Cl-] stimulate MC to release NO, a highly diffusible and rapidly acting vasodilator, provide a possible mechanism to explain the transmission of the signal for the TGF response within the JGA.


RSC Advances ◽  
2014 ◽  
Vol 4 (57) ◽  
pp. 30129-30136 ◽  
Author(s):  
Rijun Gui ◽  
Ajun Wan ◽  
Yalei Zhang ◽  
Huili Li ◽  
Tingting Zhao

This article reported the synthesis of CMC–FA–RBS(CQD) nanospheres and studied their potential applications for NO release and fluorescence imaging.


2017 ◽  
Vol 5 (36) ◽  
pp. 7519-7528 ◽  
Author(s):  
Tuanwei Liu ◽  
Jingjing Hu ◽  
Xiaoye Ma ◽  
Bing Kong ◽  
Jilan Wang ◽  
...  

Tumor targeted hollow double-layered polymer nanoparticles (HDPNs) withS-nitrosothiols for nitric oxide (NO)-release as chemotherapy were described.


1998 ◽  
Vol 85 (2) ◽  
pp. 405-410 ◽  
Author(s):  
Klaus Lewandowski ◽  
Thilo Busch ◽  
Hansjörg Lohbrunner ◽  
Susanne Rensing ◽  
Uwe Keske ◽  
...  

To investigate whether relevant levels of nasal nitric oxide (NO) are produced in the absence of paranasal sinuses, we studied 17 healthy baboons, mammals without any paranasal sinuses. The animals were anesthetized with ketamine hydrochloride and breathed spontaneously. While the baboons breathed through a face mask (mouths closed) connected to a respirator, NO concentrations in exhaled gas were sampled from the expiratory limb and analyzed by chemiluminescence. While the animals were breathing ambient air, nasal gas was sampled via a thin plastic tube and analyzed for NO concentrations by chemiluminescence. Mean NO concentration in the exhaled gas was 1.00 ± 0.59 parts/billion, and NO release was 4.28 ± 2.72 nl/min. A NO concentration of 4.79 ± 2.08 parts/billion was found in the nasal gas (NO release: 7.18 ± 3.13 nl/min). An age-dependent increase in nasal NO levels was not observed. Exhaled and nasal NO concentrations in baboons were markedly lower than in mammals with paranasal sinuses, suggesting that paranasal sinuses might be an anatomic requirement for production of relevant nasal NO levels.


2004 ◽  
Vol 287 (2) ◽  
pp. F231-F235 ◽  
Author(s):  
Marcela Herrera ◽  
Jeffrey L. Garvin

Endothelin-1 (ET-1) acutely inhibits NaCl reabsorption by the thick ascending limb (THAL) by activating the ETB receptor, stimulating endothelial nitric oxide synthase (eNOS), and releasing nitric oxide (NO). In nonrenal tissue, chronic exposure to ET-1 stimulates eNOS expression via the ETB receptor and activation of phosphatidylinositol 3-kinase (PI3K). We hypothesized that ET-1 increases eNOS expression in the THAL by binding to ETB receptors and stimulating PI3K. In primary cultures of medullary THALs treated for 24 h, eNOS expression increased by 36 ± 18% with 0.01 nM ET-1, 123 ± 30% with 0.1 nM ( P < 0.05; n = 5), and 71 ± 30% with 1 nM, whereas 10 nM had no effect. BQ-788, a selective ETB receptor antagonist, completely blocked stimulation of eNOS expression caused by 0.1 nM ET-1 (12 ± 25 vs. 120 ± 40% for ET-1 alone; P < 0.05; n = 5). BQ-123, a selective ETA receptor antagonist, did not affect the increase in eNOS caused by 0.1 nM ET-1. Sarafotoxin c (S6c; 0.1 μM), a selective ETB receptor agonist, increased eNOS expression by 77 ± 30% ( P < 0.05; n = 6). Wortmannin (0.01 μM), a PI3K inhibitor, completely blocked the stimulatory effect of 0.1 μM S6c (77 ± 30 vs. −28 ± 9%; P < 0.05; n = 6). To test whether the increase in eNOS expression heightens activity, we measured NO release in response to simultaneous treatment with l-arginine, ionomycin, and clonidine using a NO-sensitive electrode. NO release by control cells was 337 ± 61 and 690 ± 126 pA in ET-1-treated cells ( P < 0.05; n = 5). Taken together, these data suggest that ET-1 stimulates THAL eNOS, activating ETB receptors and PI3K and thereby increasing NO production.


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