Efeito da angiotensina-(1-7) na regeneração axonal e na plasticidade medular após lesão nervosa periférica

• Ano de defesa: 2015
• Autor(a) principal: Assis, Alex Dias
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Uberlândia; BR; Programa de Pós-graduação em Biologia Celular e Estrutural Aplicadas; Ciências Biomédicas; UFU
• Palavras-chave em Português: Mas; Lesão em nervo periférico; Neurônio motor; Sistema renina-angiotensina; Nervos perifericos - Doenças; Peripheral nerve injury; Motor neuron; CNPQ::CIENCIAS BIOLOGICAS::MORFOLOGIA::CITOLOGIA E BIOLOGIA CELULAR
• Link de acesso: https://repositorio.ufu.br/handle/123456789/12407; https://doi.org/10.14393/ufu.di.2015.75

After peripheral nervous injuries several modifications cellular and molecular develop to promote axonal regeneration. The axons, disconnected from their cell bodies, suffer from Wallerian degeneration. Products of this degeneration are eliminated by Schwann cells and macrophages. In the CNS, in the cell bodies, changes called plastic responses of the neuron and glia occurs in the spinal cord, highlighting the astrocytes plays an important role in this plasticity. Studies have shown that Angiotensin-(1-7), a System Renin-Angiotensin metabolite, participates in actions involving central behavioral aspects, learning and memory, by influencing the neuroplasticity. In this sense, the present work investigated the functional recovery after peripheral lesion of the sciatic nerve in rodents treated with the Ang-(1-7). For that, we procedured with the nerve crushing injury, with preservation of the epineurium. During two weeks after injury, was carried out to test the functional index of the sciatic nerve that evaluates the footprint during gait of the animals. In addition, the nerve was assessed axonal regeneration and the activity of Schwann cells by immunohistochemistry for neurofilament and S-100. In front of these results, we believe that treatment with Ang-(1-7) interferes negatively, possibly, delaying the responses of Schwann cells, which reflects a less axonal organization together with a slower return of nerve function. The lumbar spinal cords, where are the neuronal cell bodies that had their axons injured, were also stained with GFAP, synaptophysin and Mas antisera, for assessing, respectively, the astroglial activity, synaptic density and the Ang-(1-7) receptor. The treatment with Ang-(1-7) showed, in the spinal cord, reduction of the astrocytic activity and lower synaptic density after injury. Also, it was observed that the expression of Mas is changed by axonal injury, but treatment with Ang-(1-7) reduces this expression after injury by comparing the control animals with the treated animals. In this way, we can conclude that the treatment with Ang-(1-7) can influence the peripheral and central responses after nerve injury, apparently influencing the glial cells responsible, at least in part, by neuroinflammation reaction that occurs after axonal damage.