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Nitric Oxide Synthetase (nitric + oxide_synthetase)
Selected AbstractsDownregulation of inducible nitric oxide synthetase by neurotrophin-3 in microgliaJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2003Shun-Fen Tzeng Abstract Microglia activated after many neurological degeneration of the central nervous system (CNS) act as important regulators for neuropathogenesis in the injured CNS via producing proinflammatory mediators, such as nitric oxide (NO), TNF-,, and IL-1,. Neurotrophin-3 (NT-3) is a well-known trophic factor for neural survival, development, and plasticity. Activated microglia are NT-3-producing cells in the injured CNS, and express its receptor-TrkC. However, little is known about the effect of NT-3 on activated microglia. In this study, pre-treatment of a mouse microglial cell line, BV2, with NT-3 for 24 h indicated that NT-3 reduced the inducible form of NO synthase (iNOS), NO, and TNF-, in BV2 stimulated with lipopolysaccharide (LPS). NT-3 exerted less effect on the reduction of these proinflammatory mediators when it was added to BV2 cultures either simultaneously with LPS or post LPS treatment. These findings indicate that NT-3 may serve as an anti-inflammatory factor to suppress microglial activation. J. Cell. Biochem. 90: 227,233, 2003. © 2003 Wiley-Liss, Inc. [source] Radical scavenging and anti-inflammatory activity of extracts from Opuntia humifusa Raf.JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 1 2006J. Y. Cho Opuntia humifusa Raf. (O. humifusa Raf.) is a member of the Cactaceae family. To determine the antioxidative and anti-inflammatory effects of this herb, various solvent fractions (methanol, hexane, chloroform, ethyl acetate, butanol, and water) prepared from the leaves of cacti were tested using DPPH (2,2-diphenyl-l-picrylhydrazyl radical) and xanthine oxidase assays, and nitric oxide (NO)-producing macrophage cells. We found that O. humifusa Raf. displayed potent antioxidative and anti-inflammatory activity. Thus, all solvent fractions, except for the water layer, showed potent scavenging effects. The scavenging effect of the ethyl acetate fraction was higher than that of the other fractions, with IC50 values of 3.6 and 48.2 ,g mL,1. According to activity-guided fractionation, one of the active radical scavenging principles in the ethyl acetate fraction was found to be quercetin. In contrast, only two fractions (chloroform and ethyl acetate) significantly suppressed nitric oxide production from the lipopolysaccharide (LPS)-activated RAW264.7 cells. In addition, chloroform and ethyl acetate fractions significantly blocked the expression of inducible nitric oxide synthetase (iNOS) and interleukin-6 (IL-6) from the RAW264.7 cells stimulated by LPS. Moreover, ethyl acetate fractions significantly blocked the expression of IL-1, from the RAW264.7 cells stimulated by LPS. Therefore, the results suggested that O. humifusa Raf. may modulate radical-induced toxicity via both direct scavenging activity and the inhibition of reactive species generation, and the modulation of the expression of inflammatory cytokines. Finally, O. humifusa Raf. may be useful as a functional food or drug against reactive species-mediated disease. [source] 4412: Immunohistochemistry and Western blot methodologies to evaluate neuroprotective agents in models of retinopathiesACTA OPHTHALMOLOGICA, Issue 2010K THERMOS Purpose Many retinopathies that lead to visual loss and blindness are characterized by neovascularization and neural retinal defects, such as a marked loss in retinal neurons and an increase in apoptosis. There are no therapeutic agents for the treatment of the neurodegenerative component of retinal disease. Immunohistochemistry and western blot methodologies were employed to determine retinal viability and to elucidate the putative neuroprotective properties of new therapeutic targets, in animal models of retinopathy (chemical ischemia, excitotoxicity, STZ). Methods To assay retinal viability, the following antibodies for retinal markers were employed in immunohistochemical assays: PKC (rod bipolar cells), ChAT, bNOS, TH (cholinergic-, nitric oxide synthetase-, and dopamine- containing amacrine cells, respectively), calbindin-containing horizontal, amacrine and cone bipolar cells, NFL and MAP1 (ganglion axons and cells, respectively). Antibodies against various pro-survival or pro-death molecules (western blots), as well as the TUNEL-assay, were employed to examine retinal apoptosis and neuroprotection. Results Loss of retinal marker immunoreactivity was differentially observed according to the animal model employed. The neuroprotection of specific retinal neurons by the new therapeutic targets examined (somatostatin and neurosteroids) reflect the existence of protein substrates involved in the mechanism of action of these molecules. Conclusion Immunohistochemical and western blot analysis techniques provide important information on the retinal damage induced by ischemic insults and the neuroprotection afforded by new targets of retinal therapeutics. [source] Introduction on the multifaceted roles of nitric oxide in the retinaACTA OPHTHALMOLOGICA, Issue 2009NN OSBORNE Multifaceted roles of nitric oxide in the retina. N.N. Osborne. Nuffield Lab of Ophthalmology, University of Oxford, Oxford, United Kingdom Nitric oxide (NO), a free radical gas with a half-life of a few seconds is implicated in various physiological and pathophysiological roles associated with the retina and its vasculature. Generated by a family of nitric oxide synthetases (NOS), NO has been shown to bind to soluble guanylyl cyclase and to mitochondrial cytochrome c oxidase to activate defined signalling cascades. Different types of NOS exist and can be activated by calcium dependent (NOS1 and NOS3) or independent (NOS2) mechanisms. Generally, NOS1 is located to neurones while NOS2 and NOS3 are in glial and endothelial cells, respectively. NO is involved in communication between different neurones, glial cells and neurones, and in the interactions of endothelial cells with pericytes and neurones. As a consequence, a reduction in the generation of endogenous NO in the healthy retina can result in vasoconstriction; the consequences of such an affect on the retina and alterations in visual processing may alter the photoreceptor transduction mechanism and communication between retinal cells. The binding of NO to mitochondrial cytochrome c oxidase to effectively compete with oxygen has been suggested be involved in a number of processes. NO-elicited events act as triggers by which mitochondrial signal transduction cascades become involved in the induction of cellular defence mechanisms and adaptive responses. Moreover, the effect of NO on the electron transport chain might lead to mitochondrial dysfunction and pathology. NO clearly has a multifaceted role in the healthy and unhealthy retina. [source] | ||||||||||