Antihyperalgesic effects induced by the IL-1 receptor antagonist anakinra and increased IL-1β levels in inflamed and osteosarcoma-bearing mice

Baamonde, Ana; Curto-Reyes, Verdad; Juárez, Lucía; Meana, Álvaro; Hidalgo, Agustı́n; Menéndez, Luis

doi:10.1016/j.lfs.2007.07.003

Cited by 62 publications

(57 citation statements)

References 49 publications

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“…Mechanical hyperalgesia induced by osteosarcoma was blocked with 100 mg kg −1 and 300 mg kg −1 of intravenously administered anakinra (15). Nayki et al (17) studied the effects of 50 and 100 mg kg −1 doses of anakinra on ischaemic injury.…”

Section: Experimental Groupsmentioning

confidence: 99%

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The Effect of Anakinra on Paclitaxel-Induced Peripheral Neuropathic Pain in Rats

Kuyrukluyıldız¹,

Küpeli²,

Bedir³

et al. 2017

Turk J Anaesth Reanim

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Section: Experimental Groupsmentioning

confidence: 99%

“…It also inhibits the hyperalgesic response of cytokines and demonstrates antioxidant activity (14). Baamonde et al (15) reported that anakinra prevented mechanical hyperalgesia induced by osteosarcoma.…”

mentioning

confidence: 99%

The Effect of Anakinra on Paclitaxel-Induced Peripheral Neuropathic Pain in Rats

Kuyrukluyıldız¹,

Küpeli²,

Bedir³

et al. 2017

Turk J Anaesth Reanim

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“…There are many models but in general they can be attributed to three main pain groups according to their etiology: inflammatory, cancer, and neuropathic pain. Several drugs such as opioids, [1][2][3] nonsteroidal anti-inflammatory drugs (NSAIDs), 4,5 IL-1 receptor antagonist, 6 or antibodies, e.g., anti-nerve growth factor (NGF) 7 and anti-tumor necrosis factor (TNF)-α, 8 were studied in cancer pain models showing different efficacy. In neuropathic pain also opioids, [9][10][11] purinergic receptor antagonist, 12 and enkephalindegrading inhibitors 13 have been tested.…”

Section: Pain and Inflammationmentioning

confidence: 99%

IL-4, JAK-STAT signaling, and pain

Busch-Dienstfertig

González-Rodríguez

2013

JAK-STAT

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“…Furthermore, the expression of these receptors on peripheral nociceptive fibers explains the analgesia that opioids induce when acting at the periphery (Coggeshall et al 1997;Truong et al 2003). The analgesic efficacy of opioids at peripheral level has been mainly proven in experimental settings related to inflammation (Ferreira 1980;Stein et al 2003), although peripheral opioid antihyperalgesic effects have also been described in a model of murine osteosarcoma-induced hyperalgesia induced by intraosteal administration of NCTC 2472 cells (Menéndez et al 2003b(Menéndez et al , 2005(Menéndez et al , 2007Baamonde et al 2005). Data obtained by studying this model of osteosarcoma in mice seem to indicate that some nociceptive symptoms evoked by bone cancer may be inhibited by the stimulation of peripheral opioid receptors.…”

Section: Introductionmentioning

confidence: 99%

Local Loperamide Inhibits Thermal Hyperalgesia But Not Mechanical Allodynia Induced by Intratibial Inoculation of Melanoma Cells in Mice

et al. 2008

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The stimulation of peripheral opioid receptors counteracts thermal hyperalgesia produced by the intratibial inoculation of NCTC 2472 cells in mice, through the activation of the nitric oxide/cGMP/ATP-sensitive K+-channels (NO/cGMP/K(+) (ATP)) cascade (Menéndez et al. 2007, Neuropharmacology 53:71-80). We aimed to elucidate whether this peripheral opioid antihyperalgesic effect is exclusive to this model or might also occur in other types of bone neoplastic processes. In C57BL/6 mice intratibially inoculated with B16-F10 melanoma cells, the progressive tumoral damage was accompanied by the establishment of thermal hyperalgesia (unilateral hot plate test) and mechanical allodynia (von Frey test). Intraplantar administration of loperamide (15 microg, 30 min before) inhibited thermal hyperalgesia, but did not modify the intense mechanical allodynia. The fact that the coadministration of naloxone-methiodide (5 microg) completely suppressed the thermal antihyperalgesic effect induced by loperamide indicates its production through the stimulation of peripheral opioid receptors. Furthermore, its prevention by the coadministration of the non-selective inhibitor of the NO synthase, N(G)-monomethyl-L-arginine (L-NMMA, 10 microg), the selective inhibitor of neural NOS, N-omega-propyl-L-arginine (1-10 microg), or the K+ (ATP) channel blocker, glibenclamide (10 microg) demonstrated the involvement of the NO/cGMP/K(+) (ATP) pathway in the antihyperalgesic effect induced by loperamide. Overall, the present results show that the intratibial inoculation of B16-F10 cells to C57BL/6 mice evokes thermal hyperalgesia and mechanical allodynia and that, as occurred in the osteosarcoma model, the stimulation of peripheral opioid receptors is not effective in modifying neoplastic allodynia but completely inhibits thermal hyperalgesia through the activation of the NO/cGMP/K+ (ATP) cascade.

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Antihyperalgesic effects induced by the IL-1 receptor antagonist anakinra and increased IL-1β levels in inflamed and osteosarcoma-bearing mice

Cited by 62 publications

References 49 publications

The Effect of Anakinra on Paclitaxel-Induced Peripheral Neuropathic Pain in Rats

The Effect of Anakinra on Paclitaxel-Induced Peripheral Neuropathic Pain in Rats

IL-4, JAK-STAT signaling, and pain

Local Loperamide Inhibits Thermal Hyperalgesia But Not Mechanical Allodynia Induced by Intratibial Inoculation of Melanoma Cells in Mice

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