Nitric oxide and intestinal inflammation

Kubes, Paul; McCafferty, Donna–Marie

doi:10.1016/s0002-9343(00)00480-0

Cited by 313 publications

(234 citation statements)

References 75 publications

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“…Inhibition of iNOS has been shown to prevent the increase of NO production, reduce lipid peroxidation and attenuate intestinal I/R injury in the rats. 14,33 Propofol has been shown to suppress NO biosynthesis by inhibiting iNOS expression in lipopolysaccharideactivated macrophages 34 and inhibit the over-production of NO, leading to reduced vascular superoxide production and attenuated endothelial dysfunction in septic rats. 35 Further, propofol can react with peroxynitrite to form a propofol-derived phenoxyl radical, and therefore function as a peroxynitrite scavenger.…”

Section: Discussionmentioning

confidence: 99%

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Liu

Rinne

et al. 2007

Can J Anesth/J Can Anesth

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Purpose:We investigated whether propofol at a sedative dose can prevent intestinal mucosa ischemia/reperfusion (I/R) injury, and if propofol can attenuate oxidative stress and increases in nitric oxide (NO) and endothelin-1 (ET-1) release that may occur during intestinal I/R injury. Methods:Rats were randomly allocated into one of five groups (n = 10 each): (i) sham control; (ii) injury (one hour superior mesenteric artery occlusion followed by three hours reperfusion); (iii) propofol pre-treatment, with propofol given 30 min before inducing intestinal ischemia; (iv) simultaneous propofol treatment, with propofol given 30 min before intestinal reperfusion was started; (v) propofol post-treatment, with propofol given 30 min after intestinal reperfusion was initiated. In the treatment groups, propofol 50 mg·kg -1 was administrated intraperitoneally. Animals in the control and untreated injury groups received equal volumes of intralipid (the vehicle solution of propofol) intraperitoneally. Intestinal mucosa histology was analyzed by Chiu's scoring assessment. Levels of lactic acid (LD), NO, ET-1, lipid peroxidation product malondialdehyde (MDA) and superoxide dismutase (SOD) activity in intestinal mucosa were determined. Results:Histological results showed severe damage in the intestinal mucosa of the injury group accompanied by increases in MDA, NO and ET-1 and a decrease in SOD activity. Propofol treatments, especially pre-treatment, significantly reduced Chiu's scores and levels of MDA, NO, ET-1 and LD, while restoring SOD activity. Conclusion:These findings indicate that propofol attenuates intestinal I/R-induced mucosal injury in an animal model. The response may be attributable to propofol's antioxidant properties, and the effects of inhibiting over-production of NO and in decreasing ET-1 levels. CAN J ANESTH 2007 / 54: 5 / pp 366-374 Objectif : Nous avons cherché à savoir si le propofol, en dose sédative, pouvait empêcher les lésions d'ischémie/reperfusion (I/R) de la muqueuse intestinale, et s'il pouvait atténuer le stress oxydatif et les augmentations dans la libération d'oxyde nitrique (NO) et d'endothéline-1 (ET-1) pouvant survenir lors de lésions I/R intestinales. Méthode : Des rats ont été randomisés en cinq groupes (n = 10 chacun) : (i) faux témoin (sham control) ; (ii) lésion (occlusion de

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Section: Discussionmentioning

confidence: 99%

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Liu

Rinne

et al. 2007

Can J Anesth/J Can Anesth

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“…Whether endothelial cells promote or attenuate inflammatory responses to a large part seems to hinge on the level of nitric oxide (NO) production in these cells. NO is a highly potent anti-inflammatory agent that has been demonstrated to retard the progression of atherosclerosis (11) and to inhibit the development of other chronic inflammatory diseases (12).…”

Section: Interleukin-10 (Il-mentioning

confidence: 99%

Interleukin-10 Induction of Nitric-oxide Synthase Expression Attenuates CD40-mediated Interleukin-12 Synthesis in Human Endothelial Cells

Cattaruzza

Slodowski²,

Stojakovic

et al. 2003

Journal of Biological Chemistry

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“…This rapidly frees NF-B to translocate to the nucleus, where it upregulates the transcription of a variety of adhesion molecules (ICAM-1 and VCAM-1), cytokines (TNF, IL-1, and IL-6), and enzymes (iNOS; see Refs. 24 and 37).NO has been implicated as a mediator of tissue damage in several models of intestinal disease, including reperfusion injury (26,47,48). NO can be produced by three nitric oxide synthase (NOS) isoforms (neuronal NOS, iNOS, and endothelial NOS).…”

mentioning

confidence: 99%

“…NO has been implicated as a mediator of tissue damage in several models of intestinal disease, including reperfusion injury (26,47,48). NO can be produced by three nitric oxide synthase (NOS) isoforms (neuronal NOS, iNOS, and endothelial NOS).…”

mentioning

confidence: 99%

Role for complement in mediating intestinal nitric oxide synthase-2 and superoxide dismutase expression

Montalto

Hart

Jordan

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Role for complement in mediating intestinal nitric oxide synthase-2 and superoxide dismutase expression. Am J Physiol Gastrointest Liver Physiol 285: G197-G206, 2003. First published March 13, 2003 10.1152/ajpgi.00029.2003.-Inducible nitric oxide synthase (iNOS) and superoxide dismutase (SOD) play an important role in the pathology of ischemia-reperfusion. This study sought to determine if the proinflammatory effects of complement modulate iNOS and SOD in the rat after gastrointestinal ischemia and reperfusion (GI/R). An inhibitory or noninhibitory anti-complement component 5 (C5) monoclonal antibody (18A or 16C, respectively) was administered before GI/R. RT-PCR revealed a significant increase in intestinal iNOS mRNA compared with sham after GI/R that was attenuated significantly by 18A. Immunohistochemistry demonstrated increased iNOS protein expression within the intestinal crypts after GI/R. Cu/Zn SOD (mRNA and protein) was unaffected by GI/R, whereas Cu/Zn SOD activity was reduced significantly. Mn SOD protein expression was decreased significantly by GI/R. Anti-C5 preserved Cu/Zn SOD activity and Mn SOD protein expression. Staining for nitrotyrosine showed that anti-C5 treatment reduced protein nitration in the reperfused intestine. Immunohistochemistry demonstrated prominent phosphorylated (p) inhibitory factor-B (I B)-␣ staining of intestinal tissue after GI/R, whereas anti-C5 reduced p-I B-␣ expression. These data indicate that complement may mediate tissue damage during GI/R by increasing intestinal iNOS and decreasing the activity and protein levels of Cu/Zn SOD and Mn SOD, respectively. ischemia-reperfusion; inhibitory factor-B; interleukin-1␤ GASTROINTESTINAL ISCHEMIA-reperfusion (GI/R) is a common clinical problem in the settings of sepsis, hemorrhagic shock, vascular surgery, and small bowel transplantation (17, 21). GI/R causes gut dysfunction characterized by histological evidence of impaired gut motility, increased intestinal permeability, and mucosal injury (18). Numerous mediators have been implicated in GI/R injury, including cytokines (8,15,43,54,55) NF-B is maintained in a latent form in the cytoplasm of cells where it is complexed to inhibitory factor-B (I B) proteins (24). Upon activation of NF-B, I B is phosphorylated (p) by I B kinases at two conserved serine residues in the NH 2 terminus, which targets the protein for ubiquination and degradation by the proteosome. This rapidly frees NF-B to translocate to the nucleus, where it upregulates the transcription of a variety of adhesion molecules (ICAM-1 and VCAM-1), cytokines (TNF, IL-1, and IL-6), and enzymes (iNOS; see Refs. 24 and 37).NO has been implicated as a mediator of tissue damage in several models of intestinal disease, including reperfusion injury (26,47,48). NO can be produced by three nitric oxide synthase (NOS) isoforms (neuronal NOS, iNOS, and endothelial NOS). Specific inhibition of iNOS has been shown to attenuate NO production significantly and decrease intestinal injury, indicating that iNOS mediates the excessive p...

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Nitric oxide and intestinal inflammation

Cited by 313 publications

References 75 publications

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Interleukin-10 Induction of Nitric-oxide Synthase Expression Attenuates CD40-mediated Interleukin-12 Synthesis in Human Endothelial Cells

Role for complement in mediating intestinal nitric oxide synthase-2 and superoxide dismutase expression

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