Effect of Bradykinin Receptor Antagonists on Vincristine- and Streptozotocin-Induced Hyperalgesia in a Rat Model of Chemotherapy-Induced and Diabetic Neuropathy

Bujalska, Magdalena; Tatarkiewicz, Jan; Gumulka, S. W.

doi:10.1159/000110788

Cited by 25 publications

(21 citation statements)

References 49 publications

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“…Acetyl-L-carnitine can prevent mPTP opening (Pastorino et al, 1993) and is associated with a reduction in paclitaxel, oxaliplatin and bortezomib-induced CIPN when administered prophylactically in rodents (Jin et al, 2008; Bujalska and Makulska-Nowak, 2009; Carozzi et al, 2010b; Xiao et al, 2012; Zheng et al, 2012). …”

Section: Mitochondrial Dysfunction and Oxidative Stressmentioning

confidence: 99%

Pathobiology of cancer chemotherapy-induced peripheral neuropathy (CIPN)

2013

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Chemotherapy induced peripheral neuropathy (CIPN) is a type of neuropathic pain that is a major dose-limiting side-effect of potentially curative cancer chemotherapy treatment regimens that develops in a “stocking and glove” distribution. When pain is severe, a change to less effective chemotherapy agents may be required, or patients may choose to discontinue treatment. Medications used to alleviate CIPN often lack efficacy and/or have unacceptable side-effects. Hence the unmet medical need for novel analgesics for relief of this painful condition has driven establishment of rodent models of CIPN. New insights on the pathobiology of CIPN gained using these models are discussed in this review. These include mitochondrial dysfunction and oxidative stress that are implicated as key mechanisms in the development of CIPN. Associated structural changes in peripheral nerves include neuronopathy, axonopathy and/or myelinopathy, especially intra-epidermal nerve fiber (IENF) degeneration. In patients with CIPN, loss of heat sensitivity is a hallmark symptom due to preferential damage to myelinated primary afferent sensory nerve fibers in the presence or absence of demyelination. The pathobiology of CIPN is complex as cancer chemotherapy treatment regimens frequently involve drug combinations. Adding to this complexity, there are also subtle differences in the pathobiological consequences of commonly used cancer chemotherapy drugs, viz platinum compounds, taxanes, vincristine, bortezomib, thalidomide and ixabepilone, on peripheral nerves.

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Section: Mitochondrial Dysfunction and Oxidative Stressmentioning

confidence: 99%

Pathobiology of cancer chemotherapy-induced peripheral neuropathy (CIPN)

2013

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“…The vincristine-induced mechanical hyperalgesia of rats was inhibited by either the B 1 receptor antagonist des-Arg 10 -HOE 140 or the B 2 receptor antagonist HOE 140 (73).…”

Section: Role Of Bradykinin Receptors In Neuropathic Hyperalgesiamentioning

confidence: 99%

Sensory and Signaling Mechanisms of Bradykinin, Eicosanoids, Platelet-Activating Factor, and Nitric Oxide in Peripheral Nociceptors

Pethő

Reeh

2012

Physiological Reviews

241

200

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Peripheral mediators can contribute to the development and maintenance of inflammatory and neuropathic pain and its concomitants (hyperalgesia and allodynia) via two mechanisms. Activation or excitation by these substances of nociceptive nerve endings or fibers implicates generation of action potentials which then travel to the central nervous system and may induce pain sensation. Sensitization of nociceptors refers to their increased responsiveness to either thermal, mechanical, or chemical stimuli that may be translated to corresponding hyperalgesias. This review aims to give an account of the excitatory and sensitizing actions of inflammatory mediators including bradykinin, prostaglandins, thromboxanes, leukotrienes, platelet-activating factor, and nitric oxide on nociceptive primary afferent neurons. Manifestations, receptor molecules, and intracellular signaling mechanisms of the effects of these mediators are discussed in detail. With regard to signaling, most data reported have been obtained from transfected nonneuronal cells and somata of cultured sensory neurons as these structures are more accessible to direct study of sensory and signal transduction. The peripheral processes of sensory neurons, where painful stimuli actually affect the nociceptors in vivo, show marked differences with respect to biophysics, ultrastructure, and equipment with receptors and ion channels compared with cellular models. Therefore, an effort was made to highlight signaling mechanisms for which supporting data from molecular, cellular, and behavioral models are consistent with findings that reflect properties of peripheral nociceptive nerve endings. Identified molecular elements of these signaling pathways may serve as validated targets for development of novel types of analgesic drugs.

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“…79 More interestingly, simultaneous administration of indomethethacin or celecoxib with selective bradykinin B1or B2 antagonists produces an additive anti-hyperalgesic effect on the vincristine-induced neuropathic pain model, 80 whilst celecoxib alone had no effect on alleviating this type of pain. 57 These results indicate that the interaction between the activation of bradykinin receptors and cox pathways plays an important role in the development of chemotherapy-induced peripheral neuropathic pain.…”

Section: Cytokines As Candidate Biomarkers and Therapeutic Targetsmentioning

confidence: 99%

“…Pre-emptive analgesia with with lower dose of indomethacin and celecoxib significantly suppressed vincristin-induced hyperalgesia. 80-82 Therefore, the pre-emptive strategy may play an important role in prevention of peripheral neuropathic pain induced by chemotherapeutic agents.…”

Section: Cytokines As Candidate Biomarkers and Therapeutic Targetsmentioning

confidence: 99%

Discovering cytokines as targets for chemotherapy-induced painful peripheral neuropathy

et al. 2012

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Chemotherapy-induced peripheral neuropathy (CIPN), a dose-limiting neurotoxic effect of chemotherapy, is the most common reason for patients stopping their treatment early thereby increasing the risk of recurrence and decreased survival rate. Inflammatory cascade activation, proinflammatory cytokine upregulation, and neuro-immune communication play essential roles in the initiation and progression of CIPN. Most notably, TNF-α, IL-1β, IL-6, and CCL2 are involved in neuropathic pain experienced by patients undergoing chemotherapy. Further elucidation of the role of these cytokines may lead to their use as biomarkers for predicting the onset of painful peripheral neuropathy and early axonal damage. Evidence is discussed for the involvement of cytokines in CIPN, the possible underlying mechanisms, and their use as potential therapeutic targets to prevent and improve the painful peripheral neuropathy related to chemotherapeutic agents.

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Effect of Bradykinin Receptor Antagonists on Vincristine- and Streptozotocin-Induced Hyperalgesia in a Rat Model of Chemotherapy-Induced and Diabetic Neuropathy

Cited by 25 publications

References 49 publications

Pathobiology of cancer chemotherapy-induced peripheral neuropathy (CIPN)

Pathobiology of cancer chemotherapy-induced peripheral neuropathy (CIPN)

Sensory and Signaling Mechanisms of Bradykinin, Eicosanoids, Platelet-Activating Factor, and Nitric Oxide in Peripheral Nociceptors

Discovering cytokines as targets for chemotherapy-induced painful peripheral neuropathy

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