声明
TABLE OF CONTENTS
摘要
ABSTRACT
INTRODUCTION
1．0 Background
1．1 Definition of inflammatory bowel disease
1．2 The role of cytokines in IBD
1．3 The role of anti-immune cells trafficking in IBD
1．4 Challenges in IBD
1．5 Epidemiology of IBD
1．6 The role of CXCL8 (IL8) in inflammation
1．7 The structure and function of hG31P as anti-inflammatory and anti-cancer
1．8 The role of the gut mierobiome in IBD
1．9 Genetics and IBD
1．10 Problem statement of this study
1．11 Research questions
1．12 Objectives of this study
1．13 Specific objectives of this study
MATERIALS AND METHODS
2．0 Materials
2．1 Methods
2．1．0 Ethical consideration
2．1．1 Cell culture
2．1．3 ELISA assay
2．1．6 RNA extraction and cDNA amplification
2．1．7 Protein extraction and western blotting
2．1．8 Experimental subjects
2．1．9 Preparation of Lactobacillus acidophilus
2．1．10 Induction of colitis and treatment
2．1．11 Histological staining
2．1．12 Immunohistochemistry
2．1．13 Statistical analysis
RESULTS
3．1 G31P restricts THP-1 monocytes proliferation and CXCL8-CXCR1／2 expressions
3．2 G31P treatments down-regulate inflammatory cytokines expression in LPS induced inflammation of THP-1 monocytes
3．3 G31P treatment down-regulates mRNA expression of inflammatory associated enzymes and restricts monocyte-derived macrophage migration in LPS induced THP-1 cells
3．4 G31P regulates inflammatory associated transcription factors
3．5 G31P regulates inflammatory cytokines expression via AKT1，ERK1／2，and ROS pathways
3．6 G31P and G31P+LACT treatments protect against DSS induced UC
3．7 G31P and G31P+LACT treatments differentially inhibit inflammatory cytokines in DSS induced UC
3．8 G31P and G31P+LACT treatments restrict immune cells trafficking to in flamed colonin DSS induced UC
3．9 G31P and G31P+LACT treatments improved colonic fibrosis，and enhanced tight junction proteins expression in DSS induced colitis
3．10 G31P and G31P+LACT treatments modulate Egr1 and HI-1α expressions via ERK and AKTpathways respectively
DISCUSSION AND CONCLUSION
4．0 Discussion
4．0．0 In vitro
4．0．1 In vivo
4．1 Conclusion
REFERENCES
LITERATURE REVIEW
APPENDIX
ACKNOWLEDGEMENT
LIST OF PUBLICATIONS
