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Master's Dissertation
DOI
Document
Author
Full name
Victoria Regina da Silva Oliveira
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2018
Supervisor
Committee
Dale, Camila Squarzoni (President)
Marcos, Rodrigo Labat
Motta, Simone Cristina
Zambelli, Vanessa Olzon
Title in Portuguese
Estudo dos mecanismos moleculares envolvidos na analgesia induzida por tratamento com laser de baixa intensidade na neuropatia periférica diabética experimental
Keywords in Portuguese
Analgesia
Camundongo
Dor
Laser de Baixa Intensidade
Neuropatia Diabética Periférica
Abstract in Portuguese
A neuropatia periférica (NP) causada por diabetes mellitus é uma das complicações mais comuns do diabetes, atingindo cerca de 50% dos pacientes portadores da doença. Dentre os diversos sintomas da Neuropatia Periférica Diabética (NPD), destaca-se o desenvolvimento de dor crônica, que acomete, principalmente, as extremidades, manifestando-se como respostas exacerbadas para estímulos nocivos (hiperalgesia) e dor em resposta a estímulos leves ou não dolorosos (alodínia). Os tratamentos convencionais disponíveis para a neuropatia em geral, incluindo a dor associada, ainda são inadequados, insatisfatórios e beneficiam apenas uma pequena parcela dos pacientes. Na clínica, o uso de laser de baixa intensidade (LBI) torna-se cada vez mais popular, uma vez que, por promover regeneração nervosa precoce, resulta em significativa melhora das incapacidades motoras e sensitivas geradas por diversos tipos de lesões em nervos periféricos. No entanto, embora os efeitos sejam satisfatórios, os mecanismos pelos quais estes acontecem são ainda desconhecidos. Neste estudo, o efeito da laserterapia (660 nm, 30 mW, 1,6 J/cm2, 15 seg, 0.28 cm2) no tratamento da dor induzida por NPD e danos nos nervos periféricos foram avaliados em um modelo experimental de neuropatia diabética induzida por estreptozotocina em camundongos. O LBI induziu antinocicepção em camundongos com dor neuropática dependente da liberação central de opióides. Após 21 aplicações consecutivas, o LBI aumentou os níveis do fator de crescimento do nervo (NGF) e induziu a recuperação estrutural, aumentando o conteúdo mitocondrial e regulando a proteína Parkin no nervo isquiático de camundongos com NPD. Em conjunto, esses dados fornecem novos esclarecimentos sobre os mecanismos envolvidos na laserterapia, enfatizando seu potencial terapêutico no tratamento da NPD.
Title in English
Study of molecular mechanisms involved in low level laser therapy - induced analgesia in experimental Diabetic Peripheral Neuropathy.
Keywords in English
Analgesia
Diabetic Peripheral Neuropathy
Low Level Laser therapy (LLLT)
Mouse
Pain
Abstract in English
Peripheral neuropathy (PN) caused by diabetes mellitus is one of the most common complications of diabetes, affecting about 50% of patients. Among the many symptoms of Diabetic Peripheral Neuropathy (DPN), stands out the development of chronic pain, which affects mainly the extremities, presenting itself as exacerbated responses to noxious stimuli (hyperalgesia) and as pain in response to light or not painful stimuli (allodynia). Conventional treatments available for neuropathy, including the associated pain, are still inadequate, unsatisfactory and benefit only a small number of patients. In clinical practice, the low level laser therapy (LLLT) becomes increasingly popular, once it promotes early nerve regeneration, resulting in significant improvement of motor and sensory disabilities caused by various types of lesions in peripheral nerves. Although the effects are satisfactory, the mechanisms by which these effects occur are still unknown. In this study, the effects of lasertherapy (660 nm, 30 mW, 1.6 J/cm2, 15 sec, 0.28 cm2) on the treatment of DPN-induced pain and nerve damage was assessed in an experimental model of streptozotocin - induced diabetic neuropathy in mice. LLLT induced antinociception in neuropathic pain-mice dependent on the central release of opioids. After 21 consecutive applications, LLLT increased nerve growth factor (NGF) levels and induced structural recovery, increasing mitochondrial content and regulating Parkin in the sciatic nerve of mice with DPN. Together, these data provide further insights into the mechanisms involved in lasertherapy, emphasizing its therapeutic potential in the treatment of DPN.
 
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Publishing Date
2019-05-08
 
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