Orofacial sensory changes after streptozotocin-induced diabetes in rats

Nones, Carina Fernanda Mattedi; Reis, Renata Cristiane dos; Jesus, Carlos Henrique Alves; Veronez, Djanira Aparecida da Luz; Cunha, Joice Maria da; Chichorro, Juliana Geremias

doi:10.1016/j.brainres.2013.01.002

Cited by 22 publications

(11 citation statements)

References 59 publications

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“…In our data, pregabalin showed an antiallodynic effect in neonatal streptozotocin-induced diabetic rats. Concordantly, previous studies indicate that pregabalin improves orofacial and paw hyperalgesia (Nones et al, 2013;Rocha-González et al, 2014), as well as paw allodynia (Field et al, 1999;Rocha-González et al, 2014;Yamamoto et al, 2009) in diabetic rats. In addition, a meta-analysis performed using nine randomized, double-blind, placebo-controlled trials involving a total of 2056 patients indicate that pregabalin is effective to treat painful diabetic neuropathy (Zhang et al, 2015).…”

Section: Discussionsupporting

confidence: 80%

“…Pregabalin is a calcium channel α2δ subunit blocker that is approved as first-line therapy by United States, Europe, and Canada regulatory agencies for symptomatic painful diabetic peripheral neuropathy treatment (Pop-Busui et al, 2017). Pregabalin is also the most broadly studied drug in preclinical (Field, McCleary, Hughes, & Singh, 1999;Nones et al, 2013;Sałat, Librowski, Nawiesniak, & Gluch-Lutwin, 2013) and clinical studies (Freeman, Druso-De Cruz, & Emir, 2008;Pop-Busui et al, 2017;Zhang et al, 2015) in this condition, but it has moderate efficacy and limited dosage range, because it is able to cause serious side effects as blurred vision, motor incoordination, and ataxia, among others (Pop-Busui et al, 2017;Verma, Singh, & Jaggi, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Antiallodynic interaction and motor performance of the pregabalin/thioctic acid and pregabalin/α‐tocopherol combinations in neonatal streptozotocin‐induced diabetic rats

Cruz-Álvarez

Zúñiga-Romero

Huerta-Cruz

et al. 2018

Drug Development Research

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Painful peripheral neuropathy can be associated with nerve damage caused by diabetes mellitus. Although pregabalin is the first‐line therapy for peripheral neuropathy, it shows substantial discontinuation rates, mainly because of nervous system side effects as motor incoordination. Multimodal therapy may improve the motor side effect profile of pregabalin. The aim of this study was to evaluate the interaction of pregabalin + thioctic acid or pregabalin + α‐tocopherol on allodynia and motor performance in neonatal streptozotocin‐induced diabetic rats. Efficacy of drugs separately or in combination was tested by tactile allodynia using von Frey filaments. Isobolographic and interaction index analysis were used to determine the antiallodynic interaction between pregabalin and either thioctic acid or α‐tocopherol. Motor performance was measured using a rotarod test. Pregabalin, thioctic acid, and α‐tocopherol reduced, in a dose‐dependent fashion, tactile allodynia. Pregabalin + thioctic acid and pregabalin + α‐tocopherol combinations also dose‐dependently reduced allodynic behavior in diabetic rats. Isobolographic analysis revealed an additive interaction for both combinations. Consistently, the interaction indices confirmed the additive effect between pregabalin + thioctic acid and pregabalin + α‐tocopherol. In addition, the administration of either combination improved motor incoordination induced by pregabalin. Data suggests that thioctic acid or α‐tocopherol could positively impact the therapeutic profile of pregabalin, because they might be useful for reducing motor incoordination associated to pregabalin in patients with peripheral neuropathy.

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Antiallodynic interaction and motor performance of the pregabalin/thioctic acid and pregabalin/α‐tocopherol combinations in neonatal streptozotocin‐induced diabetic rats

Cruz-Álvarez

Zúñiga-Romero

Huerta-Cruz

et al. 2018

Drug Development Research

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“…The clinical evidence for the effectiveness of opioids in the control of DNP is corroborated by some pre clinical data, which have reported the effectiveness of morphine [162,163] and buprenorphine [164] in reducing thermal or mechanical hypersensitivity in DNP animal models.…”

Section: Opioidsmentioning

confidence: 76%

Diabetic neuropathic pain: Physiopathology and treatment

Schreiber

Nones

Reis

et al. 2015

WJD

353

267

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Diabetic neuropathy is a common complication of both type 1 and type 2 diabetes, which affects over 90% of the diabetic patients. Although pain is one of the main symptoms of diabetic neuropathy, its pathophysiological mechanisms are not yet fully known. It is widely accepted that the toxic effects of hyperglycemia play an important role in the development of this complication, but several other hypotheses have been postulated. The management of diabetic neuropathic pain consists basically in excluding other causes of painful peripheral neuropathy, improving glycemic control as a prophylactic therapy and using medications to alleviate pain. First line drugs for pain relief include anticonvulsants, such as pregabalin and gabapentin and antidepressants, especially those that act to inhibit the reuptake of serotonin and noradrenaline. In addition, there is experimental and clinical evidence that opioids can be helpful in pain control, mainly if associated with first line drugs. Other agents, including for topical application, such as capsaicin cream and lidocaine patches, have also been proposed to be useful as adjuvants in the control of diabetic neuropathic pain, but the clinical evidence is insufficient to support their use. In conclusion, a better understanding of the mechanisms underlying diabetic neuropathic pain will contribute to the search of new therapies, but also to the improvement of the guidelines to optimize pain control with the drugs currently available.

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“…The cornea receives a dense sensory innervation from the trigeminal ganglion (TG) (3), and corneal nerve fibers are sensitive to low-intensity mechanical, chemical, and thermal stimulation (4). The corneal nerve supports corneal epithelial nerve function (5) and plays an important role in corneal epithelial wound healing through the interactions with TG sensory neurons (6). Decreased corneal sensitivity and neuronal abnormalities in patients with diabetes were thought to be the main cause of diabetic keratopathy (7).…”

mentioning

confidence: 99%

microRNA-182 Mediates Sirt1-Induced Diabetic Corneal Nerve Regeneration

Wang

Zhao

et al. 2016

Diabetes

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Sensory neurons are particularly susceptible to neuronal damage in diabetes, and silent mating type information regulation 2 homolog 1 (Sirt1) has been recently identified as a key gene in neuroprotection and wound healing. We found that the expression of Sirt1 was downregulated in trigeminal sensory neurons of diabetic mice. A microRNA microarray analysis identified microRNA-182 (miR-182) as a Sirt1 downstream effector, and the expression level of miR-182 was increased by Sirt1 overexpression in trigeminal neurons; Sirt1 bound to the promoter of miR-182 and regulated its transcription. We also revealed that miR-182 enhanced neurite outgrowth in isolated trigeminal sensory neurons and overcame the detrimental effects of hyperglycemia by stimulating corneal nerve regeneration by decreasing the expression of one of its target genes, NOX4. Furthermore, the effects of miR-182 on corneal nerve regeneration are associated with a functional recovery of corneal sensation in hyperglycemic conditions. These data demonstrate that miR-182 is a key regulator in diabetic corneal nerve regeneration through targeting NOX4, suggesting that miR-182 might be a potential target for the treatment of diabetic sensory nerve regeneration and diabetic keratopathy.

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Orofacial sensory changes after streptozotocin-induced diabetes in rats

Cited by 22 publications

References 59 publications

Antiallodynic interaction and motor performance of the pregabalin/thioctic acid and pregabalin/α‐tocopherol combinations in neonatal streptozotocin‐induced diabetic rats

Antiallodynic interaction and motor performance of the pregabalin/thioctic acid and pregabalin/α‐tocopherol combinations in neonatal streptozotocin‐induced diabetic rats

Diabetic neuropathic pain: Physiopathology and treatment

microRNA-182 Mediates Sirt1-Induced Diabetic Corneal Nerve Regeneration

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