Effect on inducible nitric oxide

Chiu, F.L. and Lin, J.K. (2005) HPLC analysis of naturally occurring methylated catechins, 3"- and 4 -methyl-epigallocatechin gaHate, in various fresh tea leaves and commercial teas and their potent inhibitory effects on inducible nitric oxide synthase in macrophages. /. Agric. Pood Chem., 53, 7035-7042. 

Murphy P., Sharp A., Shin J., Gavrilyuk V., Dello R. C., Weinberg G., Sharp F. R., Lu A., Heneka M. T., and Feinstein D. L. (2002). Suppressive effects of ansamycins on inducible nitric oxide synthase expression and the development of experimental autoimmune encephalomyelitis. J. Neurosci. Res. 67 461 470. 

Nyska, A., Lomnitski, L., Maronpot, R., Moomaw, C., Brodsky, B., Sintov, A., Wormser, U. (2001). Effects of iodine on inducible nitric oxide synthase and cyclooxygenase-2 expression in sulfur mustard-induced skin. Arch. Toxicol. 74 768-74. 

Dirsch V, Kiemer A, Wagner H, Vollmar A. Effect of allicin and ajoene, two compounds of garlic, on inducible nitric oxide synthase. Atherosclerosis 1998 139 333-339. 

Attur MG, Patel R, Thakker G, Vyas P, Levartovsky D, Patel P, Naqvi S, Raza R, Patel K, Abramson D, Bruno G, Abramson SB, Amin AR. Differential anti-inflammatory effects of immunosuppressive drugs cyclosporin, rapamycin and FK-506 on inducible nitric oxide synthase, nitric oxide, cyclooxygenase-2 and PGE2 production. Inflamm Res 2000 49 20-26. 

Guo JS, Cheng CL, Koo MW (2004) Inhibitory effects of Centella asiatica water extract and asiaticoside on inducible nitric oxide synthase during gastric ulcer healing in rats. Planta Med 70 1150-1154... 

Exposure to trichothecenes at levels that partially inhibit translation upregulates expression of many inflammatory and immune-related genes including macrophage, Thl and Th2 cytokines as well as chemokines, cyclooxygenase 2 and inducible nitric oxide synthase.1518 Contrastingly, suppressive effects of trichothecenes on leukocyte function are intimately linked with the induction of apoptosis as has been demonstrated in macrophages, T cells and B cells both in vivo and in vitro.19-20... 

Protective effect of a novel and selective inhibitor of inducible nitric oxide synthase on experimental crescentic glomerulonephritis in WKY rats, Nephrol. Dial. Transplant. 17 (2002), p. 2117-2121... 

We have proposed a mechanism by which lL-1 exerts its deleterious effects on islet function and viability (Fig. 11 Corbett et al., 1992). In this proposed mechanism, lL-1 is released by macrophages during the initial stages of islet infiltration. IL-1 binds to a specific IL-1 receptors on the /3 cell activating a tyrosine kinase. Tyrosine kinase phosphorylation stimulates second messengers to induce the expression of c-/os, c-jun, the activation of NF-xB, and possibly other early transcriptional regulators. These early-immediate transcriptional response elements may activate or stimulate the expression of inducible nitric oxide... 

Effects of cytokines on the formation of nitric oxide by human islets as determined by EPR spectroscopy. Human islets were treated for 18 hr with 75 U/ml lL-1, 3.5 nM TNF-a, and 750 U/ml IFN-y, the islets were then isolated, and EPR spectroscopy was performed as described previously (Corbett et al., 1993b). Cytokine induced nitric oxide formation is demonstrated by the genetation of an EPR detectable g = 2.04 iton-nitrosyl complex which is prevented by 0.5 mM NMMA. Reproduced with permission from Proc. Nall. Acad. Set. U S.A. (Corbett et al., 1993b). 

Besides neuropeptides, nitric oxide is an inflammatory mediator in the airways, which is also a vasodilator and a neurotransmitter. Nitric oxide is produced by the enzymatic action of nitric oxide synthetase on L-arginine. Airways contain this enzyme in three different forms, two of which termed neuronal and endothelial nitric oxide synthetase are constitutive whereas the third form called inducible nitric oxide synthetase is inducible. The inflammatory cytokines including IL-1 and TNF-a augment the expression of inducible nitric oxide synthetase in human airway epithelial cells. Nitric oxide causes bronchodilation as a result of the relaxation of bronchial smooth muscles. It has also been suggested that nitric oxide is the neurotransmitter of the inhibitory NANC bronchodilation. The detrimental effects of nitric oxide include airway inflammation and vasodilation. It causes airway edema by increasing the erudition of plasma due to increased blood flow to postcapillary venules. The increased blood flow may also contribute to an increased mucus secretion. The role of nitric oxide in inflammatory responses has not yet been established. 

Nitric oxide may suppress THi subset and its high levels may increase the expression of TH2 subset. The action of inducible nitric oxide synthetase may result in increased exhaled nitric oxide in asthmatics. The airway epithelial cells are the predominant source of increased nitric oxide in asthmatic subjects. Since nitric oxide has both beneficial and adverse effects on bronchial airways, its precise contribution to the etiology and pathogenesis of asthmatic disease requires additional investigation. 

Yamada J, Sugimoto Y, Yoshikawa T, Horisaka K. Effects of a nitric oxide synthase inhibitor on 5-HT1A receptor agonist 8-OH-DPAT-induced hyperphagia in rats. Eur J Pharmacol 1996 316 23-26. 

Suzuki, H., Riley, R. T., and Sharma, R. P. (2007). Inducible nitric oxide has protective effect on fumonisin Bj hepatotoxicity in mice via modulation of sphingosine kinase. Toxicology 229, 42-53. 

Chatzipanteli K., Wada K., Busto R., and Dietrich W. D. (1999) Effects of moderate hypothermia on constitutive and inducible nitric oxide synthase activities after traumatic brain injury in the rat. J. Neurochem. 72, 2047-2052. 

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