| Abstract [eng] |
Glaucoma is one of the leading causes of blindness worldwide. The disease causes apoptosis of retinal ganglion cells, which are responsible for transmitting visual information signals to the brain, and degeneration of the optic nerve axons. Neurotrophic factors are involved in the preservation of these cells. One of the most important is brain-derived neurotrophic factor (BDNF). The aim of the research work was to evaluate the neuroprotective effect of BDNF in a rat optic nerve crush model using post-mortem analyses. Our aims were as following: 1. To evaluate the induction of the optic nerve crush model and the neuroprotective effect of BDNF on retinal ganglion cells by quantitative analysis of retinal ganglion cell immunohistochemical staining. 2. To assess the neuroprotective effect of BDNF in relation to the change in the expression of the selected genes that support the structure of retinal ganglion cells and regulate apoptosis. A specific retinal ganglion cell marker, RNA-binding protein with multiple splicing (RBPMS), was chosen for immunohistochemical staining and quantitative analysis. It was observed that 7 days after optic nerve crush, the number of retinal ganglion cells was reduced by 39% in the negative control intravitreal injection group (****P<0.0001 compared to healthy eyes). Meanwhile, the number of cells in the BDNF intravitreal injection treatment group decreased by only 14% (P=0.1712 compared to healthy eyes) and remained 29% (**P=0.0015) higher than the number of cells in the negative control intravitreal injection group. Two pro-apoptotic (BAX, caspase 3), two anti-apoptotic (BCL2, STAT3), and two cell structure supporting (NEFL, type I collagen) genes were selected to detect changes in gene expression. It was observed that caspase-dependent apoptosis of retinal ganglion cells was possibly activated, and NEFL gene expression was suppressed in the negative control intravitreal injection group. We conclude that BDNF treatment has a tendency to induce the expression of anti-apoptotic genes, possibly through a decrease in mitochondrial membrane permeability, and to maintain NEFL gene expression. Neither induction of the model nor treatment with BDNF induced a change in the gene expression of extracellular matrix type I collagen. |
