Eun-Mi Park
Ewha Womans University · 医学
研究室紹介
Professor Eun-Mi Park's research lab focuses on molecular mechanisms underlying oxidative stress, ischemic brain injury, and neuroprotection, with a particular emphasis on DNA damage biomarkers, inflammatory pathways, and epigenetic regulation. The lab investigates the roles of key molecules such as PARP, iNOS, STAT1, and microRNAs in cerebral ischemia and neurodegenerative processes, while also exploring therapeutic interventions using natural compounds and preconditioning strategies. Their work spans from molecular and cellular studies in animal models to translational applications in neuroinflammation and neurodegeneration. The lab integrates molecular biology, immunology, and neuroscience to identify novel targets for stroke and neurodegenerative disease treatment.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15An immunoaffinity column is described that facilitates the analysis of oxidative damage products of DNA and RNA in urine, blood plasma, and medium isolated from cultures of Escherichia coli. In intact animals, lesions (adducts) excised from DNA are transported from the cell through the circulation and excreted in urine. In bacteria, DNA adducts are excreted directly into the medium. In either case, the adducts can be assayed as a measure of oxidative damage to DNA. A monoclonal antibody that rec
Estrogens have antiinflammatory actions and protect the brain from ischemic injury. Cerebral ischemia is accompanied by an inflammatory reaction that contributes to the tissue damage, an effect mediated in part by toxic amounts of nitric oxide (NO) produced by the inducible isoform of NO synthase (iNOS). Therefore, estrogens may protect the female brain by modulating postischemic iNOS expression. To test this hypothesis, we studied whether iNOS plays a role in the mechanisms of the reduced susce
BACKGROUND AND PURPOSE: Overactivation of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP) contributes to ischemic brain injury. Because PARP upregulates proinflammatory genes, we investigated whether inducible nitric oxide synthase (iNOS), a gene involved in the deleterious effects of postischemic inflammation, participates in the mechanisms by which PARP activation contributes to cerebral ischemic injury. METHODS: The middle cerebral artery (MCA) was occluded in mice for 20 minutes usi