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重庆大学硕士学位
重庆大学硕士学位论文
英文摘要
PAGE
PAGE VI
ABSTRACT
Pathological angiogenesis is a critical event associated with formation and progression of tumor, atherosclerosis and diabetic retinopathy. On the one hand, newborn microvessels promote the development of these diseases by supplementing oxgen and nutrients. On the other hand, these microvessels exhibit defective features that are closely associated with the increase of microvascular permeability. The structural and functional abnormality, commonly characterized by absence of cell junctions and base membrane as well as peripheral cells, promotes vascular permeability and results in macromolecules extravasation. Highly permeabible vessels allow infiltration of tumor cells and inflammatory cells as well as production and local accumulation of angiogenic factors, ultimately exacerbating vessel-related diseases. Therefore, angiogenesis inhibition is proposed as a promising strategy to limit these vessel-related diseases. As the effective drug in antagonizing type II diabetes, peroxisome proliferator-activated receptor γ (PPARγ) ligand rosiglitazone is also a significant modulator of angiogenic processes and may prove to be a potential therapeutic strategy in correcting angiogenesis-related diseases. However, studies on PPARγ and the ligand rosiglitazone yielded contradictory findings with regard to its role in angiogenesis. Additionally, treatment with rosiglitazone often causes side effects like edema that are related to increased vascular permeability. Thus, the aim of this study is to identify the angiogenic and vascular permeability response to PPARγ activation by its ligand rosiglitazone. Related knowledge could pave way to safe treatment of angiogenesis-related diseases with rosiglitazone. Resusts are shown below.
Chapter one: the regulatory role and mechanism of PPARγ activation by its ligand rosiglitazone in angiogenesis
① In vivo zebrafish angiogenesis model, ex vivo rat aortic ring model and in vitro
human umbi
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