声明
前言
摘要
Introdution
ABSTRACT
Abbreviations(缩略词简表)
CONTENTS
Chapter One Effects and Mechanism of Exenatide on High Fat Diet and Chronic Stress induced Vascular Aging and Atherosclerotic Plaque Growth in ApoE-／- Mice
1．1．Introduction
1．2 materials and methods
1．2．1 Animals
1．2．2．Mouse restraint stress model
1．2．3．Preparation and quantification of atherosclerotic lesions
1．2．4．Plasma DPP4 level analysis
1．2．5．Gene expression assay
1．2．6．Histological characterization of atherosclerotic plaques
1．2．7．Gelatin zymography
1．2．9．Senescence-associated β-galactosidase(β-Gal) staining
1．2．10．ELISA and Biochemical analyses
1．2．11．Cell culture
1．2．12．Statistical analysis
1．3．1 Impact of chronic stress on body weight(Bw) and blood biological parameters
1．3．2 The chronic shress accelerated the diet-induced vascuiar aging and atherosclerotic lesion lbrmation and component change
1．3．3 The impact of the chronic stress on inflammation，oxidative stress，and proteolysis
1．3．4 The impact of tile chronic stress on the levels of plasma GLP-1，leptin and APN proteins and adipose APN gene expression
1．3．5 GLP-1R activation mitigated the HF diet-induced vascular aging and atherosclerotic plaque growth
1．3．6 The effects of exenatide on inflammation and proteolytic enzyme expression and activity
1．3．7 DPP4 inhibition increased the levels of plasma leptin and APN and the adipose APN expression in the stressed mice
1．4 Discussion
1．5 Conclusions
References
Chapter Two Clinical significance of Plasma Dipeptidy Peptidase-4 Activities in Patients with Coronary Artery Disease
2．1 Introduction
2．2 Materials and methods
2．2．1 Study population and definition
2．2．2 Plasma DPP4 activity analysis
2．2．3 Quantitative coronary angiogram (QCA)
2．2．4 Laboratory examination
2．2．5 Statistical analysis
2．3 Results
2．3．1 Patients’ laboratory and clinical characteristics
2．3．2 Atherosclerotic lesion characteristics
2．3．3 Circulating Biomarkers
2．3．4 Impacts of diabetes and CAD on plasma DPP4 activities
2．3．5 Association between DPP4 activity and CAD patients with andwithout DM
2．4 Discussion
2．4．1 DPP4 and inflammation／atherogenic lesion characterization
2．4．2 The impact of DM on plasma DPP4 levels in the CAD and non-CAD groups
2．4．3 DPP4 and lipid metabolism
2．4．4 Study limitations
2．5 Conclusion
References
综述(一) 胰高血糖素样肽1非降糖依赖抗动脉粥样硬化作用及其机制的研究进展
综述(二) 二肽基肽酶-4抑制剂非GLP-1依赖多效性及其机制的研究进展
致谢
附录
