Epilepsy is a highly prevalent, severely debilitating neurological disorder characterized by seizures and neuronal hyperactivity due to an imbalanced neurotransmission. As genetic factors play a key role in epilepsy and its treatment, various genetic and genomic technologies continue to dissect the genetic causes of this disorder. However, the exact pathogenesis of epilepsy is not fully understood, necessitating further translational studies of this condition. Here, we applied a computational in silico approach to generate a comprehensive network of molecular pathways involved in epilepsy, based on known human candidate epilepsy genes and their established molecular interactors. Clustering the resulting network identified potential key interactors that may contribute to the development of epilepsy, and revealed functional molecular pathways associated with this disorder, including those related to neuronal hyperactivity, cytoskeletal and mitochondrial function, and metabolism. While traditional antiepileptic drugs often target single mechanisms associated with epilepsy, recent studies suggest targeting downstream pathways as an alternative efficient strategy. However, many potential downstream pathways have not yet been considered as promising targets for antiepileptic treatment. Our study calls for further research into the complexity of molecular mechanisms underlying epilepsy, aiming to develop more effective treatments targeting novel putative downstream pathways of this disorder.
Aim to study the proliferative effect of various concentrations of sulfated glycosaminoglycans (sGAG) on the culture of human corneal epithelial cells. Material and methods. The study focused on the properties of a mixture of sGAG consisting of chondroitin-4-sulfate, chondroitin-6-sulfates and keratan sulfates obtained by isolation from the transparent unchanged stroma of the cornea of farm animals. The material for the in vitro study was the cells of the anterior epithelium of the human cornea. In the experimental group No.1, a mixture of sGAG was added to the culture medium at a concentration of 0.1%, in the experimental group No.2 at a concentration of 0.5%, in the experimental group No.3 at a concentration of 1.0%. In the control group No.1, the medium was replaced without the addition of solutions, cell seeding was carried out similarly to seeding with experimental samples. The negative control group included the holes of the tablet without the addition of medium and solution. Results. The highest levels of the cellular index (CI) were obtained in the experimental group No.3 (1.00% of sGAG) and amounted to 2.86 0.11 (the total increase in indicators was 60.67%). In the experimental group No.2 (0.50% sGAG), the cellular index levels were 2.650.24 (the total increase in indicators was 52.29%), which was significantly different from the experimental group No.1 (0.10% sGAG) and the control group No.1, where these indicators were 2.54 0.21 (35.81%) and 2.370.02 (25.39%) respectively. Conclusion. The final CI indicators show that solutions of the sGAG mixture at concentrations of 0.5% and 1.0% have a more pronounced proliferative effect on human corneal epithelial cells in vitro from the range of concentrations under study. The results obtained open up the prospects for the use of sGAG in the development of new approaches to the treatment of patients undergoing a chronic drug therapy or patients with concomitant corneal diseases.
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