Effects of melatonin on myelin-associated inhibitors after severe crush spinal cord injury in a mouse model

Abstract

Event Abstract Back to Event Effects of melatonin on myelin-associated inhibitors after severe crush spinal cord injury in a mouse model Kamonrapat Sompub1, Warin Krityakiarana2, Nopporn Jongkamonwiwat3, Sujira Mukda1, Pansiri Phansuwan-Pujito4 and Piyarat Govitrapong1, 5* 1 Mahidol University, Research Center for Neuroscience, Institute of Molecular Biosciences, Thailand 2 Mahidol University, Department of Rehabilitation for Person with Disabilities, Ratchasuda College, Thailand 3 Srinakharinwirot University, Division of Physical Therapy, Faculty of Health Science, Thailand 4 Srinakharinwirot University, Division of Anatomy, Faculty of Medicine, Thailand 5 Mahidol University, Center for Neuroscience and Department of Pharmacology, Faculty of Science, Thailand Spinal cord injury (SCI) remains a major impact problem in public health issue that need long term medical treatments and also rehabilitation. SCI can lead to several impairment patterns such as deteriorated motors, sensory and/or automatic dysfunction from the injury site to below the lesion. Moreover, the molecular mechanism after SCI can activate inflammation and glial scar formation via increasing of the chemokine and cytokine levels. The cascade of inflammation activates level of myelin-associated inhibitors (MAIs) formation, which ameliorated axonal regeneration at lesion site. There are numerous evidences presented that melatonin has promising effects to reduce the inflammatory signaling in central nervous system lesion. Moreover, melatonin can increase neuronal cell proliferation and/or differentiation, which also play an important role in axonal regeneration. Melatonin has been shown to have neuroprotective effect and is a good candidate for SCI treatment. This research study was aimed to evaluate the effects of melatonin on MAIs formation after SCI. Female mice (2 months old) were used in this study. There were randomly separated into 4 groups (control, SCI, SCI + melatonin and sham-operation). The SCI model was performed in spinal cord at T13-L1 level by using the severe crush injury model. In the melatonin treated group, 10 mg/kg of melatonin in ethanol was administered intraperitoneally and the spinal cord was harvested 14 days after injury. The immunohistochemistry and western blot were used to evaluate the effects of melatonin treatment. The morphology of spinal cord was observed by using antibody staining against neuronal and glial cell markers and MAIs. The results revealed that melatonin could attenuate the development of MAIs and preserve the neuron at the lesion site probably through the inhibition of cytokine system. Future study to explore this mechanism is needed. Keywords: Melatonin, in vivo, spinal cord injury, molecular mechanism, Cytokine system Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Sompub K, Krityakiarana W, Jongkamonwiwat N, Mukda S, Phansuwan-Pujito P and Govitrapong P (2016). Effects of melatonin on myelin-associated inhibitors after severe crush spinal cord injury in a mouse model. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00156 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Prof. Piyarat Govitrapong, Mahidol University, Research Center for Neuroscience, Institute of Molecular Biosciences, Salaya, Nakhonpathom, 73170, Thailand, piyarat.gov@mahidol.ac.th Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Kamonrapat Sompub Warin Krityakiarana Nopporn Jongkamonwiwat Sujira Mukda Pansiri Phansuwan-Pujito Piyarat Govitrapong Google Kamonrapat Sompub Warin Krityakiarana Nopporn Jongkamonwiwat Sujira Mukda Pansiri Phansuwan-Pujito Piyarat Govitrapong Google Scholar Kamonrapat Sompub Warin Krityakiarana Nopporn Jongkamonwiwat Sujira Mukda Pansiri Phansuwan-Pujito Piyarat Govitrapong PubMed Kamonrapat Sompub Warin Krityakiarana Nopporn Jongkamonwiwat Sujira Mukda Pansiri Phansuwan-Pujito Piyarat Govitrapong Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.