Autor: |
Binda NS; Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil. nancysbinda@yahoo.com.br., Carayon CP; Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil. charlespetruceli@hotmail.com., Agostini RM; Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil. rafaelagostini@uol.com.br., Pinheiro AC; Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil. anapinheirofar@gmail.com., Cordeiro MN; Ezequiel Dias Foundation (FUNED), Laboratory of Biochemistry, Rua Conde Pereira Carneiro 80, Belo Horizonte, Minas Gerais 30510-010, Brazil. martadonascimento.phoneutria@gmail.com., Silva MA; Faculty of Medicine, Minas Gerais Federal University, Neuroscience Laboratory, Av. Alfredo Balena 190, Belo Horizonte, Minas Gerais 30130-100, Brazil. romanosilva@gmail.com., Silva JF; Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil. jufigueira2003@yahoo.com.br., Pereira EM; Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil. elizetemrpereira@yahoo.com.br., da Silva Junior CA; Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil. claudiojunior.biologia@gmail.com., de Castro Junior CJ; Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil. celiojcjunior@gmail.com., Guimarães AL; Department of Dentistry, Montes Claros State University, University Hospital, Health Laboratory Research, Montes Claros, Montes Claros, Minas Gerais 39401-001, Brazil. andreluizguimaraes@gmail.com., Gomez MV; Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil. marcusvgomez@gmail.com. |
Abstrakt: |
The in vivo neuroprotective effect of PhTx3-4, a spider toxin N-P/Q calcium channel blocker, was studied in a rat model of NMDA-induced injury of the retina. NMDA (N-Methyl-D-Aspartate)-induced retinal injury in rats reduced the b-wave amplitude by 62% ± 3.6%, indicating the severity of the insult. PhTx3-4 treatment increased the amplitude of the b-wave, which was almost equivalent to the control retinas that were not submitted to injury. The PhTx3-4 functional protection of the retinas recorded on the ERG also was observed in the neuroprotection of retinal cells. NMDA-induced injury reduced live cells in the retina layers and the highest reduction, 84%, was in the ganglion cell layer. Notably, PhTx3-4 treatment caused a remarkable reduction of dead cells in the retina layers, and the highest neuroprotective effect was in the ganglion cells layer. NMDA-induced cytotoxicity of the retina increased the release of glutamate, reactive oxygen species (ROS) production and oxidative stress. PhTx3-4 treatment reduced glutamate release, ROS production and oxidative stress measured by malondialdehyde. Thus, we presented for the first time evidence of in vivo neuroprotection from NMDA-induced retinal injury by PhTx3-4 (-ctenitoxin-Pn3a), a spider toxin that blocks N-P/Q calcium channels. |