Title Page
Contents
Abstract 8
1. Introduction 9
2. Material and Methods 11
2.1. Materials 11
2.2. Animals 12
2.3. Immunohistochemistry 13
2.4. Cell culture 14
2.5. Oxygen/Glucose Deprevation(OGD) 15
2.6. Western blotting 16
2.7. RT-PCR 17
2.8. Protein intensity in CD31⁺ endothelial cells 18
2.9. Statistical analysis 19
3. Result 20
3.1. Detecting chronic hypoxia in the endothelial cells of retinas of Alzheimer's disease (AD). 20
3.2. Induction of HIF-1α Protein in Endothelial Cells via NOX Activation 23
3.3. NLRP3 does not appear to be the predominant inflammasome in hypoxic endothelial cells, whether in vivo or in vitro. 26
3.4. NLRP1 inflammasome is the predominant inflammasome in both in vivo and in vitro hypoxic endothelial cells. 28
3.5. Interaction Between HIF-1α and NLRP1 in In Vitro Hypoxic Endothelial Cells 31
3.6. Hypoxic microvascular cells exhibit the ASC-caspase-1-IL-1β inflammatory pathway in In vivo system. 34
4. Discussion 37
5. Conclusion 39
6. References 40
ABSTRACT(in Korean) 44
Figure 1. Investigating the Presence of Chronic Hypoxia in 16-Month-Old Triple Transgenic Mouse Models of Alzheimer's Disease (3xTg-AD). 22
Figure 2. NOX-Driven Regulation of HIF-1α Protein in Endothelial Cells. 25
Figure 3. Hypoxic endothelial cells, whether in vivo or in vitro, do not appear to express the NLRP3 inflammasome. 27
Figure 4. Hypoxic Endothelial Cells Express NLRP1 Inflammasome. 30
Figure 5. Interaction Between HIF-1α and NLRP1 in In Vitro Hypoxic Endothelial Cells. 33
Figure 6. In vivo, within the retinas of AD mice, hypoxic microvascular cells exhibit the expression of the ASC-caspase-1-IL-1β inflammation cascades. 36