بررسی مولکولی اثر پروژسترون بر کیاسمای بینایی موش صحرایی نر پس از القای دمیلیناسیون با اتیدیوم بروماید

Background and purpose: Optic neuritis is one of the appearances of Multiple Sclerosis (MS). &nbsp;Progesterone has a protective effect in central nervous system, so, in this study we aimed at investigating the effect of progesterone on myelin repair of the optic chiasm in male rats by studying the genes expression of Olig 2 (marker of oligodendrocyte precursor cells), GFAP (marker of astrocyte) and NogoA (axon growth inhibitor) following ethidium bromide-induced demyelination. Materials and methods: An experimental study was performed in which gonadectomy was conducted to remove endogenous sex hormones. Demyelination was induced by injection of 1 microliter of ethidium bromide during stereotactic surgery in the optic chiasm of rats. Then, the animals received 1mM progesterone (ICV) for 3 and 21 days. On days 3 and 21 the Olig 2, GFAP and Nogo genes expression were evaluated by RT-PCR molecular study. Results: RT-PCR analysis indicated that ethidium bromide injection increased expressions of Olig2, GFAP and Nogo-A genes especially on day 21 post demyelination induction. Progesterone treatment decreased Olig2 and GFAP genes expression (P<0.001) and Nogo-A gene expression (P<0.01) compared to the ethidium bromide group on day 21 post lesion. Conclusion: Our data demonstrated that progesterone can cause myelin repair and axon growth by decreasing the expression of inhibitory genes such as Nogo-A and GFAP and enhancing differentiation of oligodendrocyte precursor cells to oligodendrocyte. Therefore, progesterone may exert neuroprotection effect on various neurological disorders including MS.