Effects of cyclooxygenase inhibitor pretreatment on nitric oxide production, nNOS and iNOS expression in rat cerebellum

Girolamo, G Di; Farina, M; Riberio, M L; Ogando, D; Aisemberg, J; Santos, Antonio Raúl de los; Marti, M L; Franchi, A M

doi:10.1038/sj.bjp.0705771

Cited by 6 publications

(6 citation statements)

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“…Sawynok and Reid [2012] demonstrated an involvement of spinal adenosine A 1 and CB 1 cannabinoid receptors in antinociception by acetaminophen. Girolamo et al, 2003], and regulates brain opioid receptors [Orti et al, 1999]. In this study, we observed that systemic administration of naloxone reduced the antinociceptive effects of the combination, suggesting the participation of opioid pathways in the mechanisms of action of the acetaminophen-lysine clonixinate combination.…”

Section: Discussionmentioning

confidence: 50%

Naloxone Reverses the Antinociceptive Synergistic Interaction Between Acetaminophen and Lysine Clonixinate in the Formalin Test

Isiordia-Espinoza¹,

Tiznado-Orozco²,

Pozos‐Guillén

2013

Drug Development Research

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Preclinical Research The purpose of this study was to evaluate the antinociceptive interaction between acetaminophen and lysine clonixinate in the formalin test, and the possible role of opioidergic and nitric oxide pathways in the interaction. The effect of individual drugs and their combination was evaluated using the 3% formalin test in mice. Acetaminophen (31.6, 100, 178, and 316 mg/kg, i.p.) or lysine clonixinate (5.6, 10, 17.8, and 31.6 mg/kg, i.p.) were administered 10 min before formalin injection. To assess the possible mechanism(s) of action for the combination, naloxone (1 mg/kg) and N (G)‐nitro‐L‐arginine methyl ester (L‐NAME) (3 mg/kg) were used. Isobolographic analysis and the interaction index showed a synergistic effect. The experimental ED30 was lower when compared with theoretical ED30. Naloxone, but not L‐NAME, reduced the antinociceptive effect of the combination. Administration of antagonists alone did not modify formalin‐induced nociception. These data suggest that the acetaminophen–lysine clonixinate combination produces a synergistic effect involving opioid receptors.

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Section: Discussionmentioning

confidence: 50%

Naloxone Reverses the Antinociceptive Synergistic Interaction Between Acetaminophen and Lysine Clonixinate in the Formalin Test

Isiordia-Espinoza¹,

Tiznado-Orozco²,

Pozos‐Guillén

2013

Drug Development Research

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“…First, pretreatment with COX inhibitors inhibited the augmented expression of iNOS and nNOS in rat hippocampal slices treated with LPS [26]. Second, like iNOS and nNOS deficient mice, neurons in substantia nigra of COX-2 deficient mice are less prone to MPTP induced cytotoxicity than wild type mice [32].…”

Section: No and Cgmp In Neurodegenerative Diseasesmentioning

confidence: 98%

NO-cGMP Signaling and Regenerative Medicine Involving Stem Cells

Madhusoodanan

Murad

2006

Neurochem Res

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Nitric oxide (NO) is a short lived diatomic free radical species synthesized by nitric oxide synthases (NOS). The physiological roles of NO depend on its local concentrations as well as availability and the nature of downstream target molecules. At low nanomolar concentrations, activation of soluble guanylyl cyclase (sGC) is the major event initiated by NO. The resulting elevation in the intracellular cyclic GMP (cGMP) levels serves as signals for regulating diverse cellular and physiological processes. The participation of NO and cGMP in diverse physiological processes is made possible through cell type specific spatio-temporal regulation of NO and cGMP synthesis and signal diversity downstream of cGMP achieved through specific target selection. Thus cyclic GMP directly regulates the activities of its downstream effectors such as Protein Kinase G (PKG), Cyclic Nucleotide Gated channels (CNG) and Cyclic nucleotide phosphodiesterases, which in turn regulate the activities of a number of proteins that are involved in regulating diverse cellular and physiological processes. Localization and activity of the NO-cGMP signaling pathway components are regulated by G-protein coupled receptors, receptor and non receptor tyrosine kinases, phosphatases and other signaling molecules. NO also serves as a powerful paracrine factor. At micromolar concentrations, NO reacts with superoxide anion to form reactive peroxinitrite, thereby leading to the oxidation of important cellular proteins. Extensive research efforts over the past two decades have shown that NO is an important modulator of axon outgrowth and guidance, synaptic plasticity, neural precursor proliferation as well as neuronal survival. Excessive NO production as that evoked by inflammatory signals has been identified as one of the major causative reasons for the pathogenesis of a number of neurodegenerative diseases such as ALS, Alzheimers and Parkinson diseases. Regenerative therapies involving transplantation of embryonic stem cells (ES cells) and ES cell derived lineage committed neural precursor cells have recently shown promising results in animal models of Parkinson disease (PD). Recent studies from our laboratory have shown that a functional NO-cGMP signaling system is operative early during the differentiation of embryonic stem cells. The cell type specific, spatio-temporally regulated NO-cGMP signaling pathways are well suited for inductive signals to use them for important cell fate decision making and lineage commitment processes. We believe that manipulating the NO-cGMP signaling system will be an important tool for large scale generation of lineage committed precursor cells to be used for regenerative therapies.

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“…Consequently, the production of cytokines secreted by macrophages at the injury site is hampered, reducing the inflammatory response (Rainsford, 2009). Furthermore, researchers have shown that ibuprofen reduces the activity of inducible isoform of nitric oxide synthase, which produces changes in transmembrane ion flux (Liles & Flecknell, 1992) and is also involved in inflammatory processes (Di Girolamo et al, 2003). Interestingly, a study described by Da Silva et al (2011) revealed that athletes who participated in the anti-doping control of the XV Pan-American Games reported a high intake of NSAIDs during competition when compared with out-of-competition athletes.…”

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confidence: 99%

Ibuprofen intake increases exercise time to exhaustion: A possible role for preventing exercise‐induced fatigue

Lima

Stamm

Pace

et al. 2015

Scandinavian Med Sci Sports

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Although the intake of nonsteroidal anti-inflammatory drugs (NSAIDs) intake by athletes prevents soreness, little is known concerning their role in exercise performance. This study assessed the effects of ibuprofen intake on an exhaustive protocol test after 6 weeks of swimming training in rats. Animals were divided into sedentary and training groups. After training, animals were subdivided into two subsets: saline or ibuprofen. Afterwards, three repeated swimming bouts were performed by the groups. Ibuprofen (15 mg/kg) was administered once a day. Pain measurements were performed and inflammatory and oxidative stress parameters were assayed in cerebral cortex and gastrocnemius muscle. Training, ibuprofen administration, or both combined (P < 0.05; 211 ± 18s, 200 ± 31s, and 279 ± 23s) increased exercise time to exhaustion. Training decreased the acetylcholinesterase (AChE) activity (P < 0.05; 149 ± 11) in cerebral cortex. Ibuprofen intake decreased the AChE activity after exhaustive protocol test in trained and sedentary rats (P < 0.05; 270 ± 60; 171 ± 38; and 273 ± 29). It also prevented neuronal tumor necrosis factor-α (TNF-α) and interleukin (IL 1β) increase. Fatigue elicited by this exhaustive protocol may involve disturbances of the central nervous system. Additive anti-inflammatory effects of exercise and ibuprofen intake support the hypothesis that this combination may constitute a more effective approach. In addition, ergogenic aids may be a useful means to prevent exercise-induced fatigue.

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Effects of cyclooxygenase inhibitor pretreatment on nitric oxide production, nNOS and iNOS expression in rat cerebellum

Abstract: British Journal of Pharmacology (2004) 141, 1234. doi:

Cited by 6 publications

References 0 publications

Naloxone Reverses the Antinociceptive Synergistic Interaction Between Acetaminophen and Lysine Clonixinate in the Formalin Test

Naloxone Reverses the Antinociceptive Synergistic Interaction Between Acetaminophen and Lysine Clonixinate in the Formalin Test

NO-cGMP Signaling and Regenerative Medicine Involving Stem Cells

Ibuprofen intake increases exercise time to exhaustion: A possible role for preventing exercise‐induced fatigue

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