Study of the molecular mechanisms involved in the low level laser therapy-induced antinociception in experimental diabetic neuropathy

• Grant number: 15/17136-8
• Support Opportunities: Regular Research Grants
• Start date: April 01, 2016
• End date: September 30, 2018
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Camila Squarzoni Dale
• Grantee: Camila Squarzoni Dale
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated researchers: Ii-Sei Watanabe ; Vanessa Olzon Zambelli

Abstract

Peripheral neuropathy (PN) caused by diabetes mellitus is one of the most common complications of diabetes, affecting about 50% of patients with the disease. Among the many symptoms of NP, 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 treatment (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. However, although the results are satisfactory, the mechanisms by which these beneficial effects happen are still unknown. Data obtained by our group demonstrated that treatment with LBP in mice with diabetic neuropathy reverses mechanical allodynia and induces increases of NGF levels. Considering the therapeutic potential of LBP for the treatment of diabetic neuropathy, this project aims to assess the molecular mechanisms involved in the observed analgesia, with regard to: a) re-establishment of peripheral nerve ability of animals evaluated by transmission electron microscopy; b) expression of the neurotrophin BDNF, its receptor TrkB and transcription product CREB, by western blot; c) the involvement of endogenous opioid assessed by real time PCR. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

DA SILVA OLIVEIRA, VICTORIA REGINA; SANTOS-EICHLER, ROSANGELA APARECIDA; DALE, CAMILA SQUARZONI. Photobiomodulation increases cell viability via AKT activation in an in vitro model of diabetes induced by glucose neurotoxicity. Lasers in Medical Science, v. 35, n. 1, p. 149-156, FEB 2020. (16/10372-0, 15/17136-8)

ALONSO-MATIELO, HELOISA; GONCALVES, ELIZAMARA S.; CAMPOS, MARIANA; OLIVEIRA, VICTORIA R. S.; TONIOLO, ELAINE F.; ALVES, ADILSON S.; LEBRUN, IVO; DE ANDRADE, DANIEL C.; TEIXEIRA, MANOEL J.; BRITTO, LUIZ R. G.; et al. Electrical stimulation of the posterior insula induces mechanical analgesia in a rodent model of neuropathic pain by modulating GABAergic signaling and activity in the pain circuitry. Brain Research, v. 1754, MAR 1 2021. (17/25399-4, 15/17136-8, 18/18483-1, 17/07411-7, 15/23522-8)

DA SILVA OLIVEIRA, VICTORIA R.; CURY, DIEGO P.; YAMASHITA, LAURA B.; ESTECA, MARCOS V.; WATANABE, II-SEI; BERGMANN, YOKO FEE; TONIOLO, ELAINE F.; DALE, CAMILA S.. Photobiomodulation induces antinociception, recovers structural aspects and regulates mitochondrial homeostasis in peripheral nerve of diabetic mice. Journal of Biophotonics, v. 11, n. 9, SEP 2018. (16/10372-0, 15/17136-8, 14/03270-1)