European journal of pain : EJP
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Annexin 1, a glucocorticoid (GC)-inducible protein, can play an important role via formyl peptide receptor like 1 (FPR2/ALX, also known as FPRL1) in inflammatory pain modulation. The aim of this review is to analyze different lines of evidence for the role of ANXA1 with different mechanisms on inflammatory pain and describe the profile of ANXA1 as a potential analgesic. A Medline (PUBMED) search using the terms 'Annexin 1 distribution OR expression, FPR2/ALX distribution OR expression, Annexin 1 AND pain, Annexin 1 AND FPR2/ALX AND pain' was performed. ⋯ The antinociception of ANXA1 has been evaluated in diverse pain models. It has been suggested that ANXA1 may exerts its action via: (1) inhibiting vital cytokines involved in pain transmission, (2) inhibiting neutrophil accumulation through preventing transendothelial migration via an interaction with formyl peptide receptors, (3) facilitating tonic opioid release from neutrophil in inflammatory site, (4) interrupting the peripheral nociceptive transmission by suppressing neuronal excitability. In general, ANXA1 is a potential mediator for anti-nociception and the role with its receptor constitute attractive targets for developing anesthesia and analgesic drugs, and their interaction may prove to be a useful strategy to treat inflammatory pain.
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Treating bone cancer pain continues to be a major clinical challenge, and the underlying mechanisms of bone cancer pain remain elusive. Protease-activated receptor 2 (PAR2) has been reported to be involved in neurogenic inflammation, nociceptive pain and hyperalgesia. Here, we investigated the role of PAR2 in bone cancer pain development. ⋯ These findings suggest that PAR2 may be a key mediator for peripheral sensitization of bone cancer pain. Inhibiting PAR2 activation, especially during the early phase, may be a new therapy for preventing/suppressing development of bone cancer pain.
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Review
Heart rate variability and experimentally induced pain in healthy adults: A systematic review.
Reactivity of the autonomic nervous system to experimental pain stimuli has been extensively studied using measures of heart rate and blood pressure. Heart rate variability (HRV) attempts to tease out the relative contributions of sympathetic and parasympathetic activity in the autonomic control of the heart and may therefore be more appropriate to investigate autonomic response to short-term nociceptive stimulation in detail. The current evidence on HRV and experimentally induced pain has not yet been synthesized within a systematic review. ⋯ HRV has several advantages compared to other measures of autonomic reactivity in studies investigating physiological response to nociceptive stimulation. Future studies should focus on comparisons between different methods of pain induction, interindividual variability in pain sensitivity by baseline autonomic activity, and the implications of both on the use of HRV within routine clinical evaluations.
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Spinal cord injury (SCI) results in the development of chronic pain that is refractory to conventional treatment. Progesterone, a neuroprotective steroid, may offer a promising perspective in pain modulation after central injury. Here, we explore the impact of progesterone administration on the post-injury inflammatory cascade involving the enzymes cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) at the spinal cord level. We also analyse pain behaviours, the profile of glial cell activation, and IκB-α mRNA levels, as an index of NF-κB transactivation. ⋯ Our results suggest that progesterone, by modulating early neuroinflammatory events triggered after SCI, may represent a useful strategy to prevent the development of central chronic pain.
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Acacetin is a bioflavonoid with pharmacological properties such as antinociceptive/anti-inflammatory activities. However, scientific evidence of its spectrum activity and mechanisms of action is unknown. ⋯ Our data showed that systemic administration of acacetin decreased visceral and inflammatory nociception and prevented the formalin-induced oedema. In the mechanism of the acacetin antinociceptive effect, 5-HT1A, GABA/BDZs and opioid receptors but not the NO-cGMP-K(+) channel pathway seem to be involved. The data presented prove acacetin to be potentially useful in the therapy of pain-related diseases.