Enhancement of antinociception by co-administration of ibuprofen and caffeine in arthritic rats

López, José Raúl Medina; Domínguez-Ramírez, Adriana Miriam; Cook, Helgi Jung; Bravo, Gerardo Ferrando; Dı́az-Reval, Marı́a Irene; Déciga-Campos, Myrna; López‐Muñoz, Francisco

doi:10.1016/j.ejphar.2006.06.041

Cited by 36 publications

(29 citation statements)

References 29 publications

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“…The maximal adult human U.S. Food and Drug Administration approved dosage is 3200 mg=d without an adjustment for weight, equivalent to 46-64 mg=kg=d in a 50-70 kg person. The maximal tolerated dose in rats is between 240 and 375 mg=kg=d (Antezana et al, 2003;Melarange et al, 1992;Wax et al, 1975), and other neurological conditions have been treated with 56-120 mg=kg=d in rodents (Antezana et al, 2003;Fu et al, 2007;Lim et al, 2000;Lopez et al, 2006;Park et al, 2005;Richardson et al, 2005). In the studies detailed here, treatment continued for 4 weeks at a dosage of 70 mg= kg=d of ibuprofen.…”

Section: Improved Recovery From Spinal Contusion After Subacute Theramentioning

confidence: 99%

Ibuprofen Enhances Recovery from Spinal Cord Injury by Limiting Tissue Loss and Stimulating Axonal Growth

Wang

Budel

Baughman

et al. 2009

Journal of Neurotrauma

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The GTP-binding protein RhoA regulates microfilament dynamics in many cell types and mediates the inhibition of axonal regeneration by myelin and chondroitin sulfate proteoglycans. Unlike most other nonsteroidal anti-inflammatory drugs, ibuprofen suppresses basal RhoA activity (Zhou et al., 2003). A recent report suggested that ibuprofen promotes corticospinal axon regeneration after spinal cord injury (Fu et al., 2007). Here, we confirm that ibuprofen reduces ligand-induced Rho signaling and myelin-induced inhibition of neurite outgrowth in vitro. Following 4 weeks of subcutaneous administration of ibuprofen, beginning 3 days after spinal cord contusion, animals recovered walking function to a greater degree, with twice as many rats achieving a hind limb weight-bearing status. We examined the relative role of tissue sparing, axonal sprouting, and axonal regeneration in the action of ibuprofen. Histologically, ibuprofen-treated animals display an increase in spared tissue without an alteration in astrocytic or microglial reaction. Ibuprofen increases axonal sprouting from serotonergic raphespinal axons, and from rostral corticospinal fibers in the injured spinal cord, but does not permit caudal corticospinal regeneration after spinal contusion. Treatment of mice with complete spinal cord transection demonstrates long-distance raphespinal axon regeneration in the presence of ibuprofen. Thus, administration of ibuprofen improves the recovery of rats from a clinically relevant spinal cord trauma by protecting tissue, stimulating axonal sprouting, and allowing a minor degree of raphespinal regeneration.

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Section: Improved Recovery From Spinal Contusion After Subacute Theramentioning

confidence: 99%

Ibuprofen Enhances Recovery from Spinal Cord Injury by Limiting Tissue Loss and Stimulating Axonal Growth

Wang

Budel

Baughman

et al. 2009

Journal of Neurotrauma

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“…In this way, the doses of NSAIDs can be reduced as well as the number of their side effects [12]. Lopez et al [23] observed that co-administration of caffeine and ibuprofen improved the analgesic effect of ibuprofen in experimental models with laboratory animals.…”

Section: Caffeine Influence On Nsaidsmentioning

confidence: 99%

“…López et al [23] assessed the influence of different doses of caffeine on analgesic effect of various doses of ibuprofen and placebo in male Wistar rats. The median effect dose (ED 50 ) of ibuprofen administered alone amounted to approximately 22.3 mg/kg, while combined with caffeine (ED 50 ) amounted to 17.8 mg/kg for ibuprofen and 9.2 mg/kg for caffeine.…”

Section: Caffeine and Ibuprofen For Treatment Of Painmentioning

confidence: 99%

“…That effect can be observed only when at least 100 mg of caffeine is used [27]. Despite the fact that there were numerous studies trying to find out how caffeine increases the antinociceptive effect of NSAIDs and there was much evidence that caffeine increased analgesic effects, the action mechanism is still not known [23,33].…”

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confidence: 99%

“…Range) = 5-50 μg/ml, doses (d) = 200-600 mg, time to reach the peak upon extravascular administration (t max ) = 1.25 h [32]. It offers significant advantages over aspirin, indomethacin and pyrazolone derivatives, because many patients tolerate it much better [23]. It was derived from propionic acid in 1960s [1] as a non-selective inhibitor of enzyme cyclooxygenase (COX1 and COX2), which converts arachidonic acid to prostaglandins (mediators of fever and pain) and to thromboxane (stimulated production of blood clots) [31].…”

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confidence: 99%

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Review on analgesic effect of co-administrated ibuprofen and caffeine

Polski

Kasperek

Sobótka-Polska

et al. 2014

Current Issues in Pharmacy and Medical Sciences

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Pain is a symptom of many diseases and significantly affects the quality of life, so researchers are constantly seeking new substances to be used as analgesics. Other, easier way is to combine already known drugs which cause synergistic effects greater than additive, so that probability of drug-specific side effects can be reduced. Researchers showed that caffeine can be an effective analgesic adjuvant enhancing antinociceptive effect of ibuprofen in animals and humans. By using modern drug technology methods tablets containing well-soluble ibuprofen salt and caffeine can be easily prepared. Thanks to that combination, the therapeutic dose of ibuprofen can be lowered and the side effects may be reduced.

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