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DOI 10.1007/s10753-016-0399-y

Медицинская библиотека · Inflammation · 2016

Melatonin Alters the Mechanical and Thermal Hyperalgesia Induced by Orofacial Pain Model in Rats.

Scarabelot Vanessa Leal, Medeiros Liciane Fernandes, de Oliveira Carla, Adachi Lauren Naomi Spezia, de Macedo Isabel Cristina, Cioato Stefania Giotti, de Freitas Joice S, de Souza Andressa, Quevedo Alexandre, Caumo Wolnei, Torres Iraci Lucena da Silva

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Аннотация

Melatonin is a neuroendocrine hormone that presents a wide range of physiological functions including regulating circadian rhythms and sleep, enhancing immune function, sleep improvement, and antioxidant effects. In addition, melatonin has received special attention in pain treatment since it is effective and presents few adverse effects. In this study, we evaluated the effect of acute dose of melatonin upon hyperalgesia induced by complete Freund's adjuvant in a chronic orofacial pain model in Sprague-Dawley rats. Nociceptive behavior was assessed by facial Von Frey and the hot plate tests at baseline and thereafter 30, 60, and 120 min, 24 h, and 7 days after melatonin treatment. We demonstrated that acute melatonin administration alters mechanical and thermal hyperalgesia induced by an orofacial pain model (TMD), highlighting that the melatonin effect upon mechanical hyperalgesia remained until 7 days after its administration. Besides, we observed specific tissue profiles of neuroimmunomodulators linked to pain conditions and/or melatonin effect (brain-derived neurotrophic factor, nerve growth factor, and interleukins 6 and 10) in the brainstem levels, and its effects were state-dependent of the baseline of these animals.

Для цитирования: Scarabelot Vanessa Leal, Medeiros Liciane Fernandes, de Oliveira Carla, Adachi Lauren Naomi Spezia, de Macedo Isabel Cristina, Cioato Stefania Giotti, de Freitas Joice S, de Souza Andressa, Quevedo Alexandre, Caumo Wolnei, Torres Iraci Lucena da Silva. Melatonin Alters the Mechanical and Thermal Hyperalgesia Induced by Orofacial Pain Model in Rats.. Inflammation. 2016. DOI: 10.1007/s10753-016-0399-y.

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