Francisco Javier López-Muñoz

Bio: Francisco Javier López-Muñoz is an academic researcher from CINVESTAV. The author has contributed to research in topics: Analgesic & Neuropathic pain. The author has an hindex of 28, co-authored 113 publications receiving 2125 citations. Previous affiliations of Francisco Javier López-Muñoz include Instituto Politécnico Nacional & Universidad Autónoma Metropolitana.

A new model to assess analgesic activity: Pain-induced functional impairment in the rat (PIFIR)

Abstract: A new experimental model to assess analgesic activity of both analgesic and non-steroidal antiinflammatory drugs in described It uses the unilateral intra-articular knee injection of an uric acid suspension in mineral oil to produce acute inflammation, pain, and functional motor impairment The model, named “pain-induced functional impairment in the rat” (PIFIR) assesses analgesic activity by measuring the capacity to walk with the injured extremity The procedure determines both the potencies of analgesic drugs and the time course of the effect Analgesia of selected reference agents was followed for 4 h and the effect versus time curves were constructed The area under the curve (effect versus time), an expression of the overall activity during the observation period, increased in a dose-dependent manner The area under the curve, Emax, TEmax, and ED50 of reference agents tested are reported The PIFIR procedure was sensitive to opiate and nonopiate analgetics (nonsteroidal antiinflammatory drugs) and possibly steroidal antiinflammatory drugs These characteristics make it suitable for screening purposes © 1993 Wiley-Liss, Inc

Antinociceptive effect and GC/MS analysis of Rosmarinus officinalis L. essential oil from its aerial parts.

Abstract: The rationale of this investigation was to examine the antinociceptive properties of the essential oil obtained from Rosmarinus officinalis aerial parts, using a rat model of arthritic pain. The essential oil (100, 300 and 600 mg/kg, I. P.) produced a dose-dependent antinociceptive effect, manifested as a significant reduction in the dysfunction in the pain-induced functional impairment model in the rat (PIFIR model), mainly at high doses. Chemical constituents of the essential oil were further analyzed by gas chromatography-mass spectrometry (GC/MS). The major compounds in the essential oil were alpha-pinene (14.10 %), camphene (11.47 %), beta-pinene (12.02 %), myrcene (3.31 %), alpha-phellandrene (7.87 %), eucalyptol (8.58 %), 2-bornanone (3.42 %), camphor (8.75 %), isoborneol (3.48 %), borneol (4.85 %) and borneol acetate (6.49 %). The antinociceptive effects of R. officinalis essential oil were tested in combination with 0.12 mg/kg WAY100635, s. c. (an antagonist of 5-HT(1A) receptors) or 1 mg/kg naloxone, i. p. (an antagonist of endogenous opioids receptors), demonstrating in both cases an inhibition of the antinociceptive response. This study suggests an involvement, at least in part, of the serotonergic system via 5-HT(1A) receptors and endogenous opioids in the antinociceptive effect of R. officinalis essential oil in the PIFIR model.

COX-3, a cyclooxygenase-1 variant inhibited by acetaminophen and other analgesic/antipyretic drugs: Cloning, structure, and expression

Abstract: Two cyclooxygenase isozymes, COX-1 and -2, are known to catalyze the rate-limiting step of prostaglandin synthesis and are the targets of nonsteroidal antiinflammatory drugs. Here we describe a third distinct COX isozyme, COX-3, as well as two smaller COX-1-derived proteins (partial COX-1 or PCOX-1 proteins). COX-3 and one of the PCOX-1 proteins (PCOX-1a) are made from the COX-1 gene but retain intron 1 in their mRNAs. PCOX-1 proteins additionally contain an in-frame deletion of exons 5–8 of the COX-1 mRNA. COX-3 and PCOX mRNAs are expressed in canine cerebral cortex and in lesser amounts in other tissues analyzed. In human, COX-3 mRNA is expressed as an ≈5.2-kb transcript and is most abundant in cerebral cortex and heart. Intron 1 is conserved in length and in sequence in mammalian COX-1 genes. This intron contains an ORF that introduces an insertion of 30–34 aa, depending on the mammalian species, into the hydrophobic signal peptide that directs COX-1 into the lumen of the endoplasmic reticulum and nuclear envelope. COX-3 and PCOX-1a are expressed efficiently in insect cells as membrane-bound proteins. The signal peptide is not cleaved from either protein and both proteins are glycosylated. COX-3, but not PCOX-1a, possesses glycosylation-dependent cyclooxygenase activity. Comparison of canine COX-3 activity with murine COX-1 and -2 demonstrates that this enzyme is selectively inhibited by analgesic/antipyretic drugs such as acetaminophen, phenacetin, antipyrine, and dipyrone, and is potently inhibited by some nonsteroidal antiinflammatory drugs. Thus, inhibition of COX-3 could represent a primary central mechanism by which these drugs decrease pain and possibly fever.

Animal models of pain: progress and challenges

Abstract: Many are frustrated with the lack of translational progress in the pain field, in which huge gains in basic science knowledge obtained using animal models have not led to the development of many new clinically effective compounds. A careful re-examination of animal models of pain is therefore warranted. Pain researchers now have at their disposal a much wider range of mutant animals to study, assays that more closely resemble clinical pain states, and dependent measures beyond simple reflexive withdrawal. However, the complexity of the phenomenon of pain has made it difficult to assess the true value of these advances. In addition, pain studies are importantly affected by a wide range of modulatory factors, including sex, genotype and social communication, all of which must be taken into account when using an animal model.