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博碩士論文 etd-0801115-152657 詳細資訊
Title page for etd-0801115-152657
論文名稱
Title
利用體外震波改善糖尿病腎病變大鼠之腎功能
Extracorporeal shock wave therapy ameliorates kidney functions in diabetic nephropathy rat
系所名稱
Department
畢業學年期
Year, semester
語文別
Language
學位類別
Degree
頁數
Number of pages
59
研究生
Author
指導教授
Advisor
召集委員
Convenor
口試委員
Advisory Committee
口試日期
Date of Exam
2015-07-15
繳交日期
Date of Submission
2015-09-01
關鍵字
Keywords
抗發炎、組織再生、腎小球、體外震波、微量蛋白尿、糖尿病腎病變
Extracorporeal shock wave therapy, Diabetic nephropathy, Microalbuminuria, Glomerular, Tissue regeneration, Anti-inflammatory
統計
Statistics
本論文已被瀏覽 5669 次,被下載 44
The thesis/dissertation has been browsed 5669 times, has been downloaded 44 times.
中文摘要
糖尿病腎病變是糖尿病的一種併發症,糖尿病產生的高血糖環境使得腎臟過濾過多高血糖血液,時間久了腎臟功能就會異常便會開始有蛋白尿的產生。體外震波療法是一種新型的治療方法,根據之前的報導會調節抗發炎因子、抗纖維化因子、徵招幹細胞到震波治療位置。本次的研究調查體外震波治療糖尿病腎臟病大鼠是否有助於改善腎臟功能,達到組織修復的目的。本次實驗用WISTAR大鼠注射鏈脲黴素產生糖尿病,維持糖尿病症狀12周進而建立起糖尿病腎臟病大鼠模型。糖尿病腎病變大鼠具有高表現的尿中微量蛋白、腎小球肥大、細胞外基質堆積和腎小球纖維化。體外震波有效治療糖尿病腎病變大暑主要是靠去誘導自體SDF-1在損傷部位的表現量增強和徵招造血幹細胞的歸巢作用,體外震波會使在損傷部分聚集的巨噬細胞從M1期轉變成M2期,接著分泌細胞因子,如抗發炎因子來調控組織的發炎程度進而修復組織。體外震波會降低尿中微量蛋白和腎小球肥大的現象,以及減緩像前纖維化因子TGF-β、纖維化標記collagen type I、細胞凋亡標記TUNEL、發炎M1巨噬細胞標記CD68減緩這些因子的表現,而且促進增生標記物PCNA和足細胞標記WT-1的增生。總之體外震波具有調節發炎反應、抗纖維化、抗細胞凋亡、促進足細胞再生,才能恢復糖尿病腎病變大鼠的腎功能接近正常老鼠的程度。
Abstract
Diabetic nephropathy which is the most common cause of end stage renal disease continues to increase developed countries in association with the epidemic rise in diabetes. After many years, kidneys dysfunction cause to leak protein liquid in the urine. Extracorporeal shock wave therapy (ESWT) has been reported to modulate the anti-inflammatory, anti-fibrosis, and recruit mesenchymal stem cell to achieve tissue repair. This study was to investigated whether regulation of ESWT contributes to improve diabetic nephropathy in our rat model. WISTAR rats were used to induce diabetes mellitus (DM) by streptozotocin which exhibited treatment high blood glucose during 12 weeks and established DN successfully. DN rats have very high microalbuminuria, glomerular hypertrophy, Extracellular matrix accumulation and glomerular fibrosis. The treatment of Diabetic nephropathy kidneys with ESWT increases SDF-1 enhance and recruit stem cell homing and repolarise M1 macrophage to M2 macrophage secretion cytokine such as anti-inflammatory factor that repair injured tissue. ESWT decrease microalbuminuria, recover glomerular hypertrophy and attenuate expressing of pro-fibrosis maker TGF-β1, fibrosis maker collagen type I, cell apoptosis marker TUNEL assay, inflammatory marker M1 macrophages CD68, furthermore promote cell proliferation marker PCNA and podocyte marker WT-1. ESWT serves as function for immunomodulation, anti-inflammatory, anti-fibrosis,
anti-apoptosis to restore the renal functions to normal level in DN rats.
目次 Table of Contents
Acknowledgement i
Abstract in Chinese iv
Abstract in English v
Abbreviation vi
Figures and Legends viii
Introduction 1
Materials and Methods 7
General Experimental Procedures of Rat 7
Measurement of Urine Creatinine and Albumin 7
ESWT treatment 8
Immunofluorescence and Histochemistry 8
TUNEL Staining 9
Western blotting 10
Real-Time Quantitative RT-PCR Analyses of mRNA 11
ELISA Analysis 11
Statistical analysis 11
Results 13
ESWT Ameliorate Diabetes-Induced Renal Injury 13
ESWT promotes SDF-1 of expression which recruit mesenchymal stem cells to kidney 13
ESWT protect Glomeruli function resistance against Renal Injury 14
Effects of ESWT Protective Glomerular Fibrosis in Renal Injury 15
Podocyte Regeneration In ESWT Diabetes Induced Rats 16
Discussion 17
References 41
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