Effect of Etanercept, a Tumor Necrosis Factor-Alpha Inhibitor, on Neuropathic Pain in the Rat Chronic Constriction Injury Model

Zanella, J.M.; Burright, Eric N.; Hildebrand, Keith R.; Hobot, Chris; Cox, Mark; Christoferson, Laura; McKay, William F.

doi:10.1097/brs.0b013e318162340a

Cited by 57 publications

(53 citation statements)

References 69 publications

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“…Moreover, preemptive treatment with thalidomide prevented the development of STZ-induced thermal hyperalgesia and mechanical allodynia. Our results are in full agreement with Zanella et al (2008) and Dogrul et al (2011), who reported on improvement in thermal hyperalgesia with etanercept (TNF-α-antibodies). In contrast, recently, it has been reported that TNF-α elevates neurite outgrowth through an NF-κB-dependent pathway in cultured adult sensory neurons, and the diminished expression of TNF-α in diabetes may contribute to sensory neuropathy (Saleh et al 2011).…”

Section: Discussionsupporting

confidence: 95%

Effect of dipyrone and thalidomide alone and in combination on STZ-induced diabetic neuropathic pain

Chauhan

Taliyan

Sharma

2012

Naunyn-Schmiedeberg's Arch Pharmacol

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Diabetic neuropathy is recognized as one of the most common complications of chronic diabetes, but its pathophysiological mechanism is complex and yet to be completely explored. Monotherapy with conventional analgesics fails to provide adequate pain relief in peripheral diabetic neuropathy. There are a number of evidence suggesting that tumor necrosis factor (TNF-α) plays an important role in the pathogenesis of peripheral diabetic neuropathy. TNF-α up-regulation activates nuclear factor κB, which further up-regulates cyclooxygenase (COX)-2 leading to altered prostaglandin profile. Inhibition of TNF-α and COX-2 provides beneficial effect on diabetic neuropathy by decreasing the oxidative stress level and by preventing neuronal hypersensitivity due to an increased prostaglandin level. The present study was designed to assess the effect of dipyrone and thalidomide on streptozotocin (STZ)-induced neuropathic pain behavior in rats. STZ 50 mg/kg, i.p. was administered to induce experimental diabetes in the rats. Three weeks following STZ, dipyrone (300 and 600 mg/kg, i.p.) and thalidomide (25 and 50 mg/kg, i.p.) alone and subeffective dose combination of dipyrone and thalidomide (300 and 25 mg/kg(-1), i.p.) administered daily for 2 weeks significantly attenuated thermal hyperalgesia, mechanical allodynia, and formalin-induced phase-2 flinching response. Moreover, the subeffective dose combination of dipyrone and thalidomide and preemptive treatment with thalidomide (50 mg/kg) reduces oxidative stress in diabetic rats. In conclusion, the combination of subeffective dose of dipyrone and thalidomide prevented the development and maintenance of experimental diabetic neuropathy. The combination of thalidomide (TNF-α inhibitor) and dipyrone (COX inhibitor) may be used as a potential therapeutic agent for the treatment of diabetic neuropathy.

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Section: Discussionsupporting

confidence: 95%

Effect of dipyrone and thalidomide alone and in combination on STZ-induced diabetic neuropathic pain

Chauhan

Taliyan

Sharma

2012

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Both of these cytokines were shown to produce pain hypersensitivity behaviour when administered locally to the skin or into the spinal cord [110]. TNF antibodies attenuated the development of thermal hyperalgesia and mechanical allodynia in several models of neuropathic pain [35,129,172]. Other inflammatory mediators found to induce acute pain perception in vivo in humans pointing to their potential to change ion channel function were nitric oxide (on injection) and ATP (on iontophoretic application onto skin and application onto human blister base preparations) [20,68,73].…”

Section: Processes Imitating Ion Channel Dysfunction In Inflammationmentioning

confidence: 99%

Ion channels in inflammation

Eisenhut

Wallace

2011

Pflugers Arch - Eur J Physiol

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Most physical illness in vertebrates involves inflammation. Inflammation causes disease by fluid shifts across cell membranes and cell layers, changes in muscle function and generation of pain. These disease processes can be explained by changes in numbers or function of ion channels. Changes in ion channels have been detected in diarrhoeal illnesses, pyelonephritis, allergy, acute lung injury and systemic inflammatory response syndromes involving septic shock. The key role played by changes in ion transport is directly evident in inflammation-induced pain. Expression or function of all major categories of ion channels like sodium, chloride, calcium, potassium, transient receptor potential, purinergic receptor and acid-sensing ion channels can be influenced by cyto- and chemokines, prostaglandins, leukotrienes, histamine, ATP, reactive oxygen species and protons released in inflammation. Key pathways in this interaction are cyclic nucleotide, phosphoinositide and mitogen-activated protein kinase-mediated signalling, direct modification by reactive oxygen species like nitric oxide, ATP or protons and disruption of the cytoskeleton. Therapeutic interventions to modulate the adverse and overlapping effects of the numerous different inflammatory mediators on each ion transport system need to target adversely affected ion transport systems directly and locally.

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“…Recently, Zanella et al demonstrated that systemic application of etanercept reduced thermal hyperalgesia but required a 10-fold higher dose than locally administered compound in the rat constriction injury model. 53 Sommer et al reported that signifi cant decreases in thermal hyperalgesia and mechanical allodynia were seen either in local or systemic application of etanercept using chronic nerve constriction injury model. 54 These clinical and experimental fi ndings thus support the data of the present study both regarding dosage and that TNF-inhibition may reduce pain following disc rupture.…”

Section: Historical Controlsmentioning

confidence: 99%

Pharmacological Inhibition of Tumor Necrosis Factor May Reduce Pain Behavior Changes Induced by Experimental Disc Puncture in the Rat

Nakamae

Ochi

Olmarker

2011

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Effect of Etanercept, a Tumor Necrosis Factor-Alpha Inhibitor, on Neuropathic Pain in the Rat Chronic Constriction Injury Model

Abstract: This preclinical study indicates that delivering TNF-alpha inhibitors by means of a locally administered polymeric formulation provides long-lasting analgesia in an inflammatory neuropathic pain model.

Cited by 57 publications

References 69 publications

Effect of dipyrone and thalidomide alone and in combination on STZ-induced diabetic neuropathic pain

Effect of dipyrone and thalidomide alone and in combination on STZ-induced diabetic neuropathic pain

Ion channels in inflammation

Pharmacological Inhibition of Tumor Necrosis Factor May Reduce Pain Behavior Changes Induced by Experimental Disc Puncture in the Rat

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