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研究生:張鑑熹
研究生(外文):Chien-Hsi Chang
論文名稱:過度糖化最終產物在RAW264.7細胞誘導iNOS表現中蛋白質激脢C所扮演的角色
論文名稱(外文):Roles of Protein Kinase C on BSA-AGEs-Induced Nitric Oxide Synthase Expression in RAW 264.7 Macrophages
指導教授:李宏謨李宏謨引用關係
指導教授(外文):Horng-Mo Lee Ph.D.
學位類別:碩士
校院名稱:台北醫學院
系所名稱:生物醫學技術研究所
學門:醫藥衛生學門
學類:醫學技術及檢驗學類
論文種類:學術論文
論文出版年:2001
畢業學年度:89
語文別:中文
論文頁數:63
中文關鍵詞:過度糖化最終產物一氧化氮誘導性一氧化氮合成脢磷脂脢C蛋白質激脢C
外文關鍵詞:BSA-AGEsNOiNOSPLCPI-PLCPC-PLCDAGPKC
相關次數:
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中文摘要
論文名稱:過度糖化最終產物在RAW 264.7細胞誘導iNOS表現中蛋白質激脢C所扮演的角色
研究所名稱: 台北醫學大學生物醫學技術研究所
研究生姓名: 張鑑熹
畢業時間: 八十九學年度第二學期
指導教授: 李宏謨 博士 台北醫學大學生物醫學技術研究所教授
在RAW 264.7巨噬細胞中BSA-AGEs可誘導iNOS表現。本研究探討BSA-AGEs誘導iNOS表現過程中之訊息傳遞路徑,尤其是PKC異構脢在BSA-AGE誘導NO釋放及iNOS表現所扮演的角色。在RAW 264.7巨噬細胞中BSA-AGEs以具劑量和時間的依存性的誘導NO釋放和iNOS表現。tyrosine kinase 抑制劑genistein會減弱BSA-AGE誘導RAW 264.7 細胞的NO釋放和iNOS表現。除此之外,PI-PLC抑制劑U73122、PC-PLC抑制劑D609、以及PKC抑制劑,包括staurosporine、Ro 31-8220和Go 6976 都會在RAW 264.7巨噬細胞中,依不同濃度而有不同程度抑制BSA-AGE誘導NO釋放,及抑制iNOS表現,但單獨以BSA處理 RAW 264.7 細胞,不會引起iNOS表現。加入 polymyxin B(LPS 抑制劑)亦不會減弱BSA-AGEs 誘導RAW 264.7細胞之iNOS表現。PI-PLC抑制劑U73122及tyrosine kinase 抑制劑genistein皆會抑制BSA-AGEs在RAW 264.7細胞引起PIP2的水解反應。以AGEs刺激RAW 264.7細胞時,細胞內PKC-a, - b1, -d, 和-h 會從細胞質移到細胞膜。表示在RAW 264.7巨噬細胞中,PKC-a, - b1, -d, 和-h 有一種或數種參與AGEs誘導NO產生和iNOS的表現。同時 U73122、D609、及 genistein 也減弱PKC-a, -b1, -d, 和-h 的移位表現。
這些數據表示,在RAW 264.7巨噬細胞,BSA-AGEs經過上游tyrosine kinase,活化了PI-PLC和PC-PLC,產生DAG,然後活化PKC異構脢,並誘導iNOS的表現和NO的釋放。其中一種或多種PKC異構脢(-a, -b1, -d, -h )參與調控AGEs誘導iNOS表現。

Abstract
Title of Thesis: Roles of protein kinase C on BSA-AGEs-induced nitric oxide synthase expression in RAW 264.7 macrophages.
Author: Chien-Hsi Chang
Thesis advised by: Horng-Mo Lee Ph.D.
We previously found that Advanced Glycosylation End Products (AGEs) induced nitric oxide synthaseⅡ (iNOS) expression in RAW 264.7 cells. The signaling pathway involved in protein kinase C activation and the roles of PKC isoforms in AGEs-induced NO production in RAW 264.7 cells were investigated. BSA-AGEs caused a dose- and time-dependent increase in NO release and inducible NO synthase (iNOS) expression, but BSA alone did not induce iNOS expression. The polymyxin B(LPS inhibitor)also did not inhibit BSA-AGEs induced iNOS expression. The tyrosine kinase inhibitor genistein attenuated BSA-AGEs-induced NO release and iNOS expression in RAW 264.7 cells. Additionally, the phosphoinositide-specific phospholipase C (PI-PLC) inhibitor, U73122, the phosphatidylcholine-specific phospholipase C (PC-PLC) inhibitor, D609, and the PKC inhibitors including staurosporine, Ro 31-8220, and Go 6976 all inhibited the BSA-AGEs-induced iNOS expression. BSA-AGEs stimulated PIP2 turnover was attenuated by PI-PLC inhibitor, U73122 and tyrosine kinase inhibitor, genistein. Western blot analysis revealed that incubation of the RAW 264.7 cells with BSA-AGEs, results in PKC-a, -b1, -d, and -h translocation, indicating the possible involvement of one or all of PKC-a, -b1, -d, and -h in AGEs-mediated effects.
These data suggest that BSA-AGEs activate PI-PLC and PC-PLC via an upstream tyrosine kinase to induce PKC activation, then initiate the expression of iNOS and NO release. PKC isoform-a, -b1, -d, and -h were shown to be involved in the regulation of BSA-AGEs-induced iNOS expression.
縮寫詞彙
AGEs, advanced glycosylation end products.
BSA-AGEs, bovine serum albumin derived advanced glycosylation end products
NO, nitric oxide.
iNOS, inducible nitric oxide synthase.
PLC, phospholipase C.
PI-PLC, phosphoinositide-specific phospholipase C.
PC-PLC, phosphatidylcholine-specific phospholipase C.
DAG, diacylglycerol.
IP3, Inositol 1,4,5-trisphosphate.
PIP2, phosphatidylinositol 4,5-bisphosphate .
PKC, protein kinase C.
RAGE, receptor for AGEs.

目 錄
致 謝--------------------------------------------------------Ⅰ
中文摘要------------------------------------------------------Ⅱ
英文摘要------------------------------------------------------Ⅳ
縮寫詞彙------------------------------------------------------Ⅵ
目 錄--------------------------------------------------------Ⅶ
圖目錄--------------------------------------------------------Ⅸ
第一章、 前言
一、 緒論------------------------------------------------------1
二、 背景及文獻回----------------------------------------------2
(一)、過度糖化最終產物(AGEs)---------------------------------2
1. AGEs的形成--------------------------------------------------2
2. AGEs和老化疾病的關係----------------------------------------2
3. AGEs和糖尿病併發症的關係------------------------------------3
4. AGEs和Alzheimer’s disease----------------------------------5
5. RAGE------------------------------------------------------- 5
(二)、磷脂質脢C(PLC)---------------------------------------- 7
1. 簡介--------------------------------------------------------7
2. phospholipase C的活化---------------------------------------7
3. phospholipase C與iNOS的表現---------------------------------8
(三)、蛋白質激脢C(PKC)---------------------------------------9
1. PKC的分類---------------------------------------------------9
2. PKC的活化機制----------------------------------------------10
3. PKC與糖尿病併發症的關係------------------------------------11
4. PKC與細胞增生的關係----------------------------------------11
5. PKC與細胞apoptosis的關係-----------------------------------12
6. PKC與iNOS表現的關係--------------------------------------- 13
(四)、誘導性一氧化氮合成脢(iNOS)----------------------------15
1. NO的形成---------------------------------------------------15
2. NO在生理及病理上扮演的角色-------------------------------- 15
3. iNOS基因的調控表現-----------------------------------------16
第二章、 材料與實驗方法
一、 材料-----------------------------------------------------18
二、 BSA-AGEs的製備-------------------------------------------19
三、 細胞培養-------------------------------------------------19
四、 細胞數目的計數-------------------------------------------19
五、 Nitrite濃度分析------------------------------------------20
六、 phosphatidylinositol ( PI ) 水解的測定-------------------20
七、 細胞蛋白質的收集-----------------------------------------22
八、 細胞部分蛋白質的分段收集---------------------------------22
九、 蛋白質的定量---------------------------------------------23
十、 西方墨點法-----------------------------------------------23
十一、 統計學的分析-------------------------------------------24
第三章、 實驗結果---------------------------------------------25
第四章、 實驗討論---------------------------------------------50
第五章、 參考文獻---------------------------------------------53
圖目錄
圖一(A)、 BSA-AGEs依劑量依存性誘導NO產生--------------------26
圖一(B)、 BSA-AGEs依劑量依存性誘導iNOS表現------------------27
圖二(A)、 BSA-AGEs依時間依存性誘導NO產生--------------------28
圖二(B)、 BSA-AGEs依時間依存性誘導iNOS表現----------------- 29
圖三(A)、 Polymyxin B不會抑制BSA-AGEs 誘導iNOS的表現--------31
圖三(B)、 Polymyxin B抑制LPS誘導iNOS的表現------------------31
圖四 (A)、 Genistein抑制BSA-AGEs誘導NO的產生-----------------33
圖四 (B)、 U73122抑制BSA-AGEs誘導NO的產生--------------------34
圖四 (C)、 D609會抑制BSA-AGEs誘導NO的產生--------------------35
圖四(D)、 Genistein、U73122、D609抑制BSA-AGEs誘導iNOS的
表現----------------------------------------------------------36
圖五 (A)、 BSA-AGEs依時間依存性引起[3H]-inositolmonophosphate的累積----------------------------------------------------------38
圖五 (B)、 BSA-AGEs依時間依存性引起[3H]-IP2 + [3H]-IP3的累積-39
圖六(A)、 BSA-AGEs引起[3H]-inositol monophosphate 的累積會被
U73122及genistein所減弱---------------------------------------40
圖六(B)、 BSA-AGEs引起[3H]-IP2 + [3H]-IP3的累積會被U73122
及genistein所減弱---------------------------------------------41
圖七、 在RAW 264.7 細胞,BSA-AGEs會促使 PKC-a、-b1、-d、-h
由細胞質移位到細胞膜------------------------------------------43
圖八(A)、 PKC 抑制劑staurosporine抑制BSA-AGEs誘導NO的產生-- 44
圖八(B)、 PKC 抑制劑Ro 31-8220抑制BSA-AGEs誘導NO的產生----- 45
圖八(C)、 PKC 抑制劑Go 6976抑制BSA-AGEs誘導NO的產生-------- 46
圖八 (D)、 PKC 抑制劑staurosporine、Ro 31-8220、Go 6976抑制BSA-AGEs誘導iNOS的表現--------------------------------------------47
圖九、 U73122、D609、genistein抑制PKC-a、-b1、-d、-h 由細胞質移位到細胞膜------------------------------------------------49

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