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Seiji Ito - One of the best experts on this subject based on the ideXlab platform.
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the anti inflammatory drug Sodium Salicylate inhibits nitric oxide formation induced by interleukin 1β at a translational step but not at a transcriptional step in hepatocytes
Hepatology, 1997Co-Authors: Kazushige Sakitani, Hiroaki Kitade, K Inoue, Yasuo Kamiyama, Mikio Nishizawa, Tadayoshi Okumura, Seiji ItoAbstract:Recent evidence suggests that nitric oxide (NO) mediates cellular injury under the pathological conditions such as endotoxemia in the liver of rats. Regulation of NO production is crucial for improving the hepatic dysfunction. We have previously reported that, in cultured rat hepatocytes, a single cytokine interleukin-1β (IL-1β) stimulated a release of nitrite, an oxidation product of NO, into culture medium dose- and time-dependently. The objective of this study was to investigate an ability of the anti-inflammatory drug NaSA to affect the production of NO in hepatocytes. IL-1β increased levels of inducible NO synthase (iNOS) messenger RNA (mRNA) with a maximal effect at 8 hours in primary cultures of rat hepatocytes. Nuclear factor-κB (NF-κB), that is an important nuclear factor protein in iNOS gene transcription in response to inflammatory mediators, also appeared in the nuclear fraction of hepatocytes 1 hour after addition of IL-1β. Sodium Salicylate markedly inhibited the NO formation induced by IL-1β, but did not affect NF-κB activation and iNOS mRNA induction. Western blot analysis revealed that Sodium Salicylate (NaSA) blocked a step of iNOS protein synthesis. These findings indicate that NaSA may reduce hepatic injury by preventing the induction of NO formation in response to IL-1β at the posttranscriptional step.
Michael D Apley - One of the best experts on this subject based on the ideXlab platform.
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analgesic efficacy of Sodium Salicylate in an amphotericin b induced bovine synovitis arthritis model
Journal of Dairy Science, 2009Co-Authors: J L Kotschwar, Johann F Coetzee, David E Anderson, R Gehring, Butch Kukanich, Michael D ApleyAbstract:This study examined the efficacy of Sodium Salicylate for providing analgesia in an amphotericin B-induced bovine synovitis-arthritis model using 10 male Holstein calves, 4 to 6 mo old and weighing approximately 250 kg. The study used a repeated measures partial crossover design with 2 phases, consisting of 3 treatment periods within each phase. Calves were blocked by body weight and randomly assigned to the Sodium Salicylate (50 mg/kg i.v.) or placebo group for phase 1. In period 1, lameness induction was simulated with a needle prick of the coronary band, followed by drug or placebo administration. At predetermined time points, serial blood samples for cortisol and Salicylate concentrations, electrodermal activity measurements, heart rates, and pressure mat data were collected. Visual lameness scores were recorded by an observer blinded to treatments. In period 2, lameness was induced with injection of amphotericin B into the distal interphalangeal joint, followed by drug or placebo administration, with sample collection as described previously. In period 3, the drug or placebo was administered to the respective calves with sample collection. After a 10-d washout period, phase 2 was conducted with treatments crossed over between groups. Cortisol and Salicylate samples were analyzed by competitive chemiluminescent immunoassay and fluorescence polarization immunoassay, respectively. The pharmacokinetic data were analyzed using compartmental analysis. Mean intravenous Salicylate apparent volume of distribution was 0.2 +/- 0.005 L/kg, total body clearance was 4.3 +/- 0.2 mL/min.kg, and elimination half-life was 36.9 +/- 1.2 min. The repeated measures data were analyzed based on a univariate split-plot approach with a random effects-mixed model. Differences in stance phase duration and serum cortisol concentration values were seen both between periods and between treatment group x periods; differences in heart rate, contact surface area, and contact pressure values were seen between periods, suggesting that our lameness model was effective. No differences were seen between treatment groups. When analyzed by visual lameness score, differences were seen in heart rate, contact surface area, contact pressure, and cortisol concentrations. Area under the time-effect curves, determined by using the trapezoidal rule, had results similar to the repeated measures data, except for a difference in period for electrodermal activity. This amphotericin B-induced synovitis-arthritis model is a useful tool for studying changes associated with lameness in cattle. Sodium Salicylate was not effective in providing analgesia after lameness.
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attenuation of acute plasma cortisol response in calves following intravenous Sodium Salicylate administration prior to castration
Journal of Veterinary Pharmacology and Therapeutics, 2007Co-Authors: Johann F Coetzee, R Gehring, Butch Kukanich, Aaron Bettenhausen, Brian V Lubbers, S E Toerber, Daniel U Thomson, Michael D ApleyAbstract:Pain associated with castration in cattle is an animal welfare concern in beef production. This study examined the effect of oral aspirin and intravenous (i.v.) Sodium Salicylate on acute plasma cortisol response following surgical castration. Twenty bulls, randomly assigned to the following groups, (i) uncastrated, untreated controls, (ii) castrated, untreated controls, (iii) 50 mg/kg Sodium Salicylate i.v. precastration and (iv) 50 mg/kg aspirin (acetylsalicylic acid) per os precastration, were blood sampled at 3, 10, 20, 30, 40, 50 min and 1, 1.5, 2, 4, 6, 8, 10 and 12 h postcastration. Samples were analyzed by competitive chemiluminescent immunoassay and fluorescence polarization immunoassay for cortisol and Salicylate, respectively. Data were analyzed using noncompartmental analysis, a simple cosine model, anova and t-tests. Intravenous Salicylate V(d(ss)) was 0.18 L/kg, Cl(B) was 3.36 mL/min/kg and t(1/2 lambda) was 0.63 h. Plasma Salicylate concentrations above 25 microg/mL coincided with significant attenuation in peak cortisol concentrations (P = 0.029). Peak Salicylate concentrations following oral aspirin administration was <10 microg/mL and failed to attenuate cortisol response. Once Salicylate concentrations decreased below 5 microg/mL, cortisol response in the castrated groups was significantly higher than uncastrated controls (P = 0.018). These findings have implications for designing drug regimens to provide analgesia during routine animal husbandry procedures.
Johann F Coetzee - One of the best experts on this subject based on the ideXlab platform.
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effect of intravenous Sodium Salicylate administration prior to castration on plasma cortisol and electroencephalography parameters in calves
Journal of Veterinary Pharmacology and Therapeutics, 2011Co-Authors: Luciana Bergamasco, Johann F Coetzee, Ronette Gehring, L Murray, T Song, R A MosherAbstract:Bergamasco, L., Coetzee, J. F., Gehring, R., Murray, L., Song, T., Mosher, R. A. Effect of intravenous Sodium Salicylate administration prior to castration on plasma cortisol and electroencephalography parameters in calves. J. vet. Pharmacol. Therap. 34, 565–576. Nociception is an unavoidable consequence of many routine management procedures such as castration in cattle. This study investigated electroencephalography (EEG) parameters and cortisol levels in calves receiving intravenous Sodium Salicylate in response to a castration model. Twelve Holstein calves were randomly assigned to the following groups: (i) castrated, untreated controls, (ii) 50 mg/kg Sodium Salicylate IV precastration, were blood sampled at 0, 5, 10, 20, 30, 45, 60, 90, 120, 150, 180, 240, 360, and 480 min postcastration. The EEG recording included baseline, castration, immediate recovery (0–5 min after castration), middle recovery (5–10 min after castration), and late recovery (10–20 min after castration). Samples were analyzed by competitive chemiluminescent immunoassay and fluorescence polarization immunoassay for cortisol and Salicylate, respectively. EEG visual inspection and spectral analysis were performed. Statistical analyses included anova repeated measures and correlations between response variable. No treatment effect was noted between the two groups for cortisol and EEG measurements, namely an attenuation of acute cortisol response and EEG desynchronization in Sodium Salicylate group. Time effects were noted for EEG measurements, cortisol and Salicylates levels. Significant correlations between cortisol and EEG parameters were noted. These findings have implications for designing effective analgesic regimens, and they suggest that EEG can be useful to monitor pain attributable to castration.
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analgesic efficacy of Sodium Salicylate in an amphotericin b induced bovine synovitis arthritis model
Journal of Dairy Science, 2009Co-Authors: J L Kotschwar, Johann F Coetzee, David E Anderson, R Gehring, Butch Kukanich, Michael D ApleyAbstract:This study examined the efficacy of Sodium Salicylate for providing analgesia in an amphotericin B-induced bovine synovitis-arthritis model using 10 male Holstein calves, 4 to 6 mo old and weighing approximately 250 kg. The study used a repeated measures partial crossover design with 2 phases, consisting of 3 treatment periods within each phase. Calves were blocked by body weight and randomly assigned to the Sodium Salicylate (50 mg/kg i.v.) or placebo group for phase 1. In period 1, lameness induction was simulated with a needle prick of the coronary band, followed by drug or placebo administration. At predetermined time points, serial blood samples for cortisol and Salicylate concentrations, electrodermal activity measurements, heart rates, and pressure mat data were collected. Visual lameness scores were recorded by an observer blinded to treatments. In period 2, lameness was induced with injection of amphotericin B into the distal interphalangeal joint, followed by drug or placebo administration, with sample collection as described previously. In period 3, the drug or placebo was administered to the respective calves with sample collection. After a 10-d washout period, phase 2 was conducted with treatments crossed over between groups. Cortisol and Salicylate samples were analyzed by competitive chemiluminescent immunoassay and fluorescence polarization immunoassay, respectively. The pharmacokinetic data were analyzed using compartmental analysis. Mean intravenous Salicylate apparent volume of distribution was 0.2 +/- 0.005 L/kg, total body clearance was 4.3 +/- 0.2 mL/min.kg, and elimination half-life was 36.9 +/- 1.2 min. The repeated measures data were analyzed based on a univariate split-plot approach with a random effects-mixed model. Differences in stance phase duration and serum cortisol concentration values were seen both between periods and between treatment group x periods; differences in heart rate, contact surface area, and contact pressure values were seen between periods, suggesting that our lameness model was effective. No differences were seen between treatment groups. When analyzed by visual lameness score, differences were seen in heart rate, contact surface area, contact pressure, and cortisol concentrations. Area under the time-effect curves, determined by using the trapezoidal rule, had results similar to the repeated measures data, except for a difference in period for electrodermal activity. This amphotericin B-induced synovitis-arthritis model is a useful tool for studying changes associated with lameness in cattle. Sodium Salicylate was not effective in providing analgesia after lameness.
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attenuation of acute plasma cortisol response in calves following intravenous Sodium Salicylate administration prior to castration
Journal of Veterinary Pharmacology and Therapeutics, 2007Co-Authors: Johann F Coetzee, R Gehring, Butch Kukanich, Aaron Bettenhausen, Brian V Lubbers, S E Toerber, Daniel U Thomson, Michael D ApleyAbstract:Pain associated with castration in cattle is an animal welfare concern in beef production. This study examined the effect of oral aspirin and intravenous (i.v.) Sodium Salicylate on acute plasma cortisol response following surgical castration. Twenty bulls, randomly assigned to the following groups, (i) uncastrated, untreated controls, (ii) castrated, untreated controls, (iii) 50 mg/kg Sodium Salicylate i.v. precastration and (iv) 50 mg/kg aspirin (acetylsalicylic acid) per os precastration, were blood sampled at 3, 10, 20, 30, 40, 50 min and 1, 1.5, 2, 4, 6, 8, 10 and 12 h postcastration. Samples were analyzed by competitive chemiluminescent immunoassay and fluorescence polarization immunoassay for cortisol and Salicylate, respectively. Data were analyzed using noncompartmental analysis, a simple cosine model, anova and t-tests. Intravenous Salicylate V(d(ss)) was 0.18 L/kg, Cl(B) was 3.36 mL/min/kg and t(1/2 lambda) was 0.63 h. Plasma Salicylate concentrations above 25 microg/mL coincided with significant attenuation in peak cortisol concentrations (P = 0.029). Peak Salicylate concentrations following oral aspirin administration was <10 microg/mL and failed to attenuate cortisol response. Once Salicylate concentrations decreased below 5 microg/mL, cortisol response in the castrated groups was significantly higher than uncastrated controls (P = 0.018). These findings have implications for designing drug regimens to provide analgesia during routine animal husbandry procedures.
Kazushige Sakitani - One of the best experts on this subject based on the ideXlab platform.
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the anti inflammatory drug Sodium Salicylate inhibits nitric oxide formation induced by interleukin 1β at a translational step but not at a transcriptional step in hepatocytes
Hepatology, 1997Co-Authors: Kazushige Sakitani, Hiroaki Kitade, K Inoue, Yasuo Kamiyama, Mikio Nishizawa, Tadayoshi Okumura, Seiji ItoAbstract:Recent evidence suggests that nitric oxide (NO) mediates cellular injury under the pathological conditions such as endotoxemia in the liver of rats. Regulation of NO production is crucial for improving the hepatic dysfunction. We have previously reported that, in cultured rat hepatocytes, a single cytokine interleukin-1β (IL-1β) stimulated a release of nitrite, an oxidation product of NO, into culture medium dose- and time-dependently. The objective of this study was to investigate an ability of the anti-inflammatory drug NaSA to affect the production of NO in hepatocytes. IL-1β increased levels of inducible NO synthase (iNOS) messenger RNA (mRNA) with a maximal effect at 8 hours in primary cultures of rat hepatocytes. Nuclear factor-κB (NF-κB), that is an important nuclear factor protein in iNOS gene transcription in response to inflammatory mediators, also appeared in the nuclear fraction of hepatocytes 1 hour after addition of IL-1β. Sodium Salicylate markedly inhibited the NO formation induced by IL-1β, but did not affect NF-κB activation and iNOS mRNA induction. Western blot analysis revealed that Sodium Salicylate (NaSA) blocked a step of iNOS protein synthesis. These findings indicate that NaSA may reduce hepatic injury by preventing the induction of NO formation in response to IL-1β at the posttranscriptional step.
Rainer Amann - One of the best experts on this subject based on the ideXlab platform.
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anti inflammatory effects of aspirin and Sodium Salicylate
European Journal of Pharmacology, 2002Co-Authors: Rainer Amann, B A PeskarAbstract:Abstract Aspirin (acetylsalicylic acid) is one of the most widely used drugs worldwide. It acetylates cyclooxygenases thereby irreversibly blocking the conversion of arachidonic acid to prostanoids. Biotransformation of aspirin yields Salicylate, a compound that possesses similar anti-inflammatory potency as aspirin but lacks aspirin's inhibitory effect on the activity of isolated cyclooxygenase. This article is aimed at providing an overview about the often conflicting results concerning the mechanisms of action of aspirin and Sodium Salicylate. At present, there is no common agreement about the extent to which Salicylate contributes to aspirin's anti-inflammatory properties, as well as there is still no final conclusion reached about the mechanisms of action of Sodium Salicylate. Several possible sites of action of Salicylate have been suggested: It has been shown that in intact cells—but not in purified enzyme preparations—, Sodium Salicylate inhibits prostanoid biosynthesis. This effect seems to be prevented in the presence of high concentrations of arachidonic acid, which has been shown to interfere with inhibition by Salicylate of cyclooxygenase-2-mediated prostanoid formation in vitro. Other possible sites of action that are not directly related to cyclooxygenase inhibition have been suggested based on observations made in vitro using high concentrations of aspirin and Sodium Salicylate. These effects target intracellular signaling mechanisms such as kinases, including the mitogen activated protein-kinases (MAPK) cascade. With the exception of reported Salicylate-induced activation of p38 MAPK, observed effects are usually inhibitory. This may be one reason for the observation that, downstream to kinases, inhibitory effects of Salicylates have been observed on several nuclear transcription factors, such as nuclear transcription factor kappa B (NF-kB) or activator protein 1 (AP-1). Several reports have also shown interference by Salicylates with the expression of cyclooxygenase-2, which, depending on experimental models, can be observed as inhibitory but also stimulatory effects. Antioxidant properties of Salicylates, adenosine release induced by Sodium Salicylate and aspirin-triggered lipoxin formation are additional mechanisms that may contribute to anti-inflammatory properties of aspirin and/or Sodium Salicylate. An additional focus of this review is the discussion of interactions between aspirin, Sodium Salicylate and other non-steroidal anti-inflammatory drugs (NSAIDs), which are of particular relevance in the gastro-intestinal and cardiovascular systems.
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inhibition of carrageenan induced edema by indomethacin or Sodium Salicylate does not prevent the increase of nerve growth factor in the rat hind paw
Neuroscience Letters, 2000Co-Authors: Rainer Amann, Rufina SchuligoiAbstract:It is known that the concentration of nerve growth factor (NGF) is increased in inflamed tissue, a phenomenon thought to induce long-lasting sensitization of afferent neurons. Although the effects of NGF may be of pathophysiological relevance, there is little known about the effects of non-steroidal anti-inflammatory drugs on the inflammation-induced increase in NGF. In the present study, therefore, we used the non-steroidal anti-inflammatory drugs indomethacin and Sodium Salicylate in carrageenan-induced rat paw inflammation, in order to compare their anti-inflammatory action (determined as inhibition of edema) with their effects on the concentration of NGF in inflamed tissue. Carrageenan-induced inflammation increased the concentration of NGF in the paw 2-fold compared to non-inflamed controls. Indomethacin (0.66–2 mg/kg) and Sodium Salicylate (100–300 mg/kg) inhibited carrageenan-induced paw edema and indomethacin also inhibited the ex-vivo release of immunoreactive prostaglandin E2 from inflamed paw skin. However, at these doses, neither anti-inflammatory agent reduced the elevated levels of NGF. In contrast, a supramaximal dose of indomethacin (6 mg/kg) partially inhibited, and dexamethasone completely prevented the carrageenan-induced increase in NGF. These results suggest that the anti-inflammatory potency of drugs as determined in the carrageenan edema model is not necessarily predictive for their ability to inhibit the NGF response. It seems possible, therefore, that even if anti-inflammatory treatment prevents the appearance of visible signs of inflammation, there may be still long-lasting effects of NGF on the phenotype of primary afferent neurons.