M2 polarize mikroglia kökenli eksozomal miR-191-5p'nin oksidatif stres aracılı nöronal hasar üzerindeki nöroprotektif etkilerinin incelenmesi

Microglia, as resident cells of the brain, are involved in the maintenance of the neuronal environment by activating the response mechanism during brain damage. There are two types of microglial activation: "classically activated" M1 or "alternatively activated" M2 polarization. M2 polarization is described as the "curative" phenotype. M2 polarized microglial cells exert their neuroprotective roles by phagocytosis of neuron debris and secretion of trophic factors. However, the mechanism by which M2 microglia perform its neuroprotective function is largely unknown. Exosomes are extracellular vesicles that are released into the intercellular environment by different cell types and can cross the blood-brain barrier. Exosomes play a role in cell-cell communication and that exosome cargo can contain microRNAs (miRNAs), proteins, and mRNAs (messenger RNAs), which can be stably transferred to the recipient cell. It has been revealed that exosomal miRNA may have a neuroprotective role during injury. Hydrogen peroxide (H2O2) is encountered in the central nervous system as a reactive oxygen species (ROS). In case of excessive storage in the cell, it causes oxidative stress. Neuronal cells are prone to oxidative stress due to their high oxygen metabolism. Therefore, ROS-induced damage is encountered in the pathogenesis of many neurodegenerative diseases. The aim of this thesis study is to examine the neuroprotective effects of M2 microglia-derived exosomal miR-191-5p on the H2O2-induced neuron damage model in SH-SY5Y cells. As a result of the study, it was determined that the neuroprotective effects of M2 microglia-derived exosomes on neuronal cells under oxidative stress were mediated by miR-191-5p.