Antinociceptive profiles of aspirin and acetaminophen in formalin, substance P and glutamate pain models

Choi, Seong-Soo; Lee, Jin-Koo; Suh, Hong‐Won

doi:10.1016/s0006-8993(01)03126-2

Cited by 88 publications

(52 citation statements)

References 26 publications

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“…The acetic acidinduced writhing response is considered as a visceral inflammatory pain model (Koster and Beer 1959). Formalin pain model is widely agreed that the nociceptive behaviors manifested during the acute first phase and tonic second phase (Hunskaar et al 1985;Choi et al 2001). We found in the present study that the pain stimulation induced by acetic acid and formalin increases the blood glucose level in a fasting group.…”

Section: Discussionsupporting

confidence: 61%

Various pain stimulations cause an increase of the blood glucose level

Sim

Park

Kang

et al. 2012

Animal Cells and Systems

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The relationship between pain stimulation and the blood glucose level was studied in ICR mice. We examined the possible change of the blood glucose level after the pain stimulation induced by acetic acid injected intraperitoneally (i.p.),, formalin injected subcutaneously (s.c.) into the hind paw, or substance P (SP), glutamate, and proinflammatory cytokines (TNF-a and IFN-g) injected intrathecally (i.t.). We found in the present study that acetic acid, formalin, SP, TNF-a, and IFN-g increased the blood glucose level. The blood glucose level reached at maximal state 30 min and returned to normal level 2 h after the pain stimulation in a fasting group. Furthermore, acetic acid, formalin, SP, TNF-a, and IFN-g caused the elevation of the blood glucose level in D-glucose-fed group only in an additive manner. However, i.t. injection of glutamate did not alter the blood glucose level in a fasting group. In contrast, i.t. injection of glutamate enhanced the blood glucose level in the D-glucose-fed group. Our results suggest that the blood glucose level appears to be differentially regulated by various pain stimulation induced by acetic acid, formalin, SP, glutamate, and pro-inflammatory cytokines.

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Section: Discussionsupporting

confidence: 61%

Various pain stimulations cause an increase of the blood glucose level

Sim

Park

Kang

et al. 2012

Animal Cells and Systems

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“…As well as, other organoselenium compounds (Jesse et al, 2007Pavin et al, 2011;Pinto et al, 2008;Savegnago et al, 2007a,c;Wilhelm et al, 2009), the BMD reduced the nociceptive response induced by glutamate in mice. Of note, aspirin and acetaminophen demonstrated an antinociceptive effect in the glutamate test (Choi et al, 2001). Beirith et al (2002) demonstrated that nociception induced by glutamate is greatly mediated by the release of NO.…”

Section: Discussionmentioning

confidence: 99%

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Donato

Pavin

Goes

et al. 2014

Pharmaceutical Biology

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(2015) Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action, Pharmaceutical Biology, 53:3, 395-403, DOI: 10.3109/13880209.2014 -nitro-L-arginine ( L-NOARG), but the effect of BMD was not abolished by naloxone. Mechanical hyperalgesia induced by Cg and CFA was attenuated by BMD, 70 ± 4% and 65 ± 4%, respectively. Furthermore, a single oral dose of BMD did not change plasma aspartate (AST) and alanine aminotransferase (ALT) activities or urea and creatinine levels. Conclusion: BMD demonstrated as a promising compound because of the antinociceptive and anti-hyperalgesic properties in mice.

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“…1b). APAP is thought to produce analgesia primarily by acting at central sites [10][11][12] and intraplantar injection of APAP (100 µg and 500 µg) had no effect on either hot plate latency or paw-pressure withdrawal threshold in wild-type mice (Fig. 1c,d).…”

Section: The Antinociceptive Effect Of Apap Requires Trpa1mentioning

confidence: 99%

TRPA1 mediates spinal antinociception induced by acetaminophen and the cannabinoid Δ9-tetrahydrocannabiorcol

et al. 2011

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TRPA1 is a unique sensor of noxious stimuli and, hence, a potential drug target for analgesics. Here we show that the antinociceptive effects of spinal and systemic administration of acetaminophen (paracetamol) are lost in Trpa1 − / − mice. The electrophilic metabolites N-acetylp-benzoquinoneimine and p-benzoquinone, but not acetaminophen itself, activate mouse and human TRPA1. These metabolites also activate native TRPA1 and, as a consequence, reduce voltage-gated calcium and sodium currents in primary sensory neurons. The N-acetyl-pbenzoquinoneimine metabolite l-cysteinyl-S-acetaminophen was detected in the mouse spinal cord after systemic acetaminophen administration. In the hot-plate test, intrathecal administration of N-acetyl-p-benzoquinoneimine, p-benzoquinone and the electrophilic TRPA1 activator cinnamaldehyde produced antinociception that was lost in Trpa1 − / − mice. Intrathecal injection of a non-electrophilic cannabinoid, ∆ 9 -tetrahydrocannabiorcol, also produced TRPA1-dependent antinociception in this test. our study provides a molecular mechanism for the antinociceptive effect of acetaminophen and discloses spinal TRPA1 activation as a potential pharmacological strategy to alleviate pain.

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Antinociceptive profiles of aspirin and acetaminophen in formalin, substance P and glutamate pain models

Cited by 88 publications

References 26 publications

Various pain stimulations cause an increase of the blood glucose level

Various pain stimulations cause an increase of the blood glucose level

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

TRPA1 mediates spinal antinociception induced by acetaminophen and the cannabinoid Δ9-tetrahydrocannabiorcol

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