Peripheral nitric oxide in carrageenan-induced inflammation

Omote, Keiichi; Hazama, Kazuaki; Kawamata, Tomoyuki; Kawamata, Mikito; Nakayaka, Yoshito; Toriyabe, Masaki; Namiki, Akiyoshi

doi:10.1016/s0006-8993(01)02733-0

Cited by 106 publications

(58 citation statements)

References 21 publications

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“…Carrageenin increased concentrations of NO 2 /NO 3 in the dialysate measured by a subcutaneously implanted microdialysis probe. Locally applied L-NMMA or denervation of the sciatic nerve suppressed the carrageenininduced increase in NO 2 /NO 3 (Omote et al, 2001). …”

Section: Acupuncture Axon Reflex and Neurogenic Inflammationmentioning

confidence: 90%

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

2003

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Section: Acupuncture Axon Reflex and Neurogenic Inflammationmentioning

confidence: 90%

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

2003

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“…CARV (100 mg ⁄ kg) was able to block both phases of the formalin response but its effect was more prominent in the second phase. Intraplantar injection of formalin has been described to induce the production and release of NO [41], which in turn is suggested to be an essential component of the pro-inflammatory ⁄ nociceptive response by the stimulation of the production and release of cytokines, ROS and prostanoids [34,42]. Scavenging activity by CARV on NO and other reactive species may be an important mechanism of the antinociceptive action by this molecule.…”

Section: Discussionmentioning

confidence: 99%

Bioassay‐guided Evaluation of Antioxidant and Antinociceptive Activities of Carvacrol

Guimarães

Oliveira

Melo

et al. 2010

Basic Clin Pharma Tox

192

135

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We examined the antioxidant properties in vitro and the antinociceptive effect of carvacrol (CARV) in several models of pain in mice. CARV presented a strong antioxidant potential according to the TRAP ⁄ TAR evaluation; it also presented scavenger activity against nitric oxide and prevented lipid peroxidation in vitro. In mice, when evaluated against acetic acidinduced abdominal writhing, CARV (25, 50 and 100 mg ⁄ kg, i.p.) reduced (p < 0.001) the number of writhing compared to the control group, without opioid participation. In the formalin test, CARV also significantly inhibited both the early (neurogenic pain) and the late (inflammatory pain) phases of formalin-induced licking, with inhibition percentage values of 56.8% (100 mg ⁄ kg) for the neurogenic phase and 41.2% (25 mg ⁄ kg), 73.8% (50 mg ⁄ kg) and 99.7% (100 mg ⁄ kg) for the inflammatory phase. CARV also produced a significant inhibition of the pain caused by capsaicin (63.1, 67.1 and 95.8%, p < 0.001) and glutamate (46.4, 61.4 and 97.9%, p < 0.01). When assessed in a thermal model of pain, CARV (100 mg ⁄ kg, i.p.) caused a significant increase (p < 0.05) in the latency response on the hot-plate test. Such results were unlikely to be provoked by motor abnormality. Together, these results indicate that the properties of CARV should be more thoroughly examined in order to achieve newer tools for management and ⁄ or treatment of painful conditions, including those related to pro-oxidant states.

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“…Intraplantar injection of an iNOS inhibitor enhanced the mechanical hyperalgesia induced by carrageenan (72). In carrageenan-induced rat paw inflammation, an increase in nNOS activity (in both phases) and appearance of iNOS activity (in the late phase) were revealed along with enhanced levels of NO metabolites (nitrite/nitrate) in the paw exudate (109,266,550,624,729). Carrageenan-induced heat hyperalgesia was not altered in iNOS-deficient mice (712).…”

Section: Peripheral Antinociceptive Effects/roles Of Nitric Oxidementioning

confidence: 96%

Sensory and Signaling Mechanisms of Bradykinin, Eicosanoids, Platelet-Activating Factor, and Nitric Oxide in Peripheral Nociceptors

Pethő

Reeh

2012

Physiological Reviews

241

200

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Peripheral mediators can contribute to the development and maintenance of inflammatory and neuropathic pain and its concomitants (hyperalgesia and allodynia) via two mechanisms. Activation or excitation by these substances of nociceptive nerve endings or fibers implicates generation of action potentials which then travel to the central nervous system and may induce pain sensation. Sensitization of nociceptors refers to their increased responsiveness to either thermal, mechanical, or chemical stimuli that may be translated to corresponding hyperalgesias. This review aims to give an account of the excitatory and sensitizing actions of inflammatory mediators including bradykinin, prostaglandins, thromboxanes, leukotrienes, platelet-activating factor, and nitric oxide on nociceptive primary afferent neurons. Manifestations, receptor molecules, and intracellular signaling mechanisms of the effects of these mediators are discussed in detail. With regard to signaling, most data reported have been obtained from transfected nonneuronal cells and somata of cultured sensory neurons as these structures are more accessible to direct study of sensory and signal transduction. The peripheral processes of sensory neurons, where painful stimuli actually affect the nociceptors in vivo, show marked differences with respect to biophysics, ultrastructure, and equipment with receptors and ion channels compared with cellular models. Therefore, an effort was made to highlight signaling mechanisms for which supporting data from molecular, cellular, and behavioral models are consistent with findings that reflect properties of peripheral nociceptive nerve endings. Identified molecular elements of these signaling pathways may serve as validated targets for development of novel types of analgesic drugs.

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Peripheral nitric oxide in carrageenan-induced inflammation

Cited by 106 publications

References 21 publications

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

Bioassay‐guided Evaluation of Antioxidant and Antinociceptive Activities of Carvacrol

Sensory and Signaling Mechanisms of Bradykinin, Eicosanoids, Platelet-Activating Factor, and Nitric Oxide in Peripheral Nociceptors

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