Investigation of the neuroprotective roles of drugs effective on epigenetic mechanisms on neuroinflammation cell model

Chlamydia pneumoniae (Cpn) is a mandatory intracellular gram-negative pathogen that causes a wide variety of pulmonary diseases, usually mild and atypical. Cpn can cause permanent infections, and there is growing evidence about the role in the pathology of Alzheimer's disease (AD). In this thesis, the effects of Cpn infection and drugs, that are effective on epigenetic mechanisms, Trichostatin A (TSA), givinostat, and RG108 and an antibiotic rifampin, on the neuronal microenvironment related genes related to inflammatory and epigenetic chromatin regulation were investigated with gene panels. In addition, the neuroprotective effects of the drugs on amyloid beta (Aβ) (1-42)-induced neurotoxicity model were investigated by evaluating the cell viability with the real-time cell analysis system and determining the Aβ1-42 antibody, total ROS and apoptotic effect levels using flow cytometer. As a result, especially TSA and RG108 have been found neuroprotective on both neuroinflammation and neurotoxicity models. In addition, on the newly introduced Cpn-induced neuroinflammation model, the relationship between TSA, RG108, givinostat and rifampin with AD was investigated in the context of epigenetic and inflammatory effects, and significant expression changes were determined in SETD7, DPEP2, HDAC10, HDAC4, SETD8, RAGE and RELA genes. It is believed that the results provide preliminary data on epigenetic disorders in AD neuropathology and neuroprotective action mechanisms against Aβ neurotoxicity, which may constitute an alternative step to AD treatment that has limited therapeutic options.