INVESTIGATION OF TRANSCRIPTOMIC, PROTEOMIC, AND ENZYMATIC ACTIVITY PROFILE OF LIVER ANTIOXIDANT ENZYMES (CAT, SOD, GPx, Trx) IN MULTIPLE SCLEROSIS MICE MODEL

2023-12-28
Gjota Ergin, Sena
Multiple Sclerosis (MS) is an inflammatory and demyelinating disease of the central nervous system (CNS) and it is usually observed in early adulthood. In order to analyze MS, its clinical and pathological features are reflected in animals by creating Experimental Autoimmune Encephalomyelitis (EAE) model. The aim of the present study is to investigate the transcriptomic, proteomic, and enzymatic activity profile of liver antioxidant enzymes in mice EAE model. Liver is the major organ containing a variety of enzymes needed for drug metabolism hence it is important to study antioxidant enzymes in MS mice model. To address this issue, this study has analyzed the liver antioxidant enzymes in RNA level by transcriptome and qRT- PCR, in protein level by Western Blot and enzyme activity assays. The results obtained from transcriptome showed no difference in catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and thioredoxin (Trx) between EAE and control group. In qRT-PCR, CAT and GPx showed significant difference between EAE and control group. In western blot, only Trx showed decrease in EAE compared to control group whereas other enzymes showed no difference between the groups. In enzymatic activity, CAT and Trx showed increase, GPx showed decrease and SOD showed no change between EAE and control group. Post- trancriptional/post-translational modifications may affect enzymatic differences between EAE and control groups. Lastly, further transcriptomic analysis showed top 14 upregulated and 3 downregulated pathways and top 15 upregulated and 14 downregulated genes.
Citation Formats
S. Gjota Ergin, “INVESTIGATION OF TRANSCRIPTOMIC, PROTEOMIC, AND ENZYMATIC ACTIVITY PROFILE OF LIVER ANTIOXIDANT ENZYMES (CAT, SOD, GPx, Trx) IN MULTIPLE SCLEROSIS MICE MODEL,” Ph.D. - Doctoral Program, Middle East Technical University, 2023.