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研究生:曹心薇
研究生(外文):Hsin-Wei Tsao
論文名稱:葉綠素衍生物光動力治療誘發人類肝癌Huh-7細胞死亡之機制探討
論文名稱(外文):The Mechanism of Photodynamic Therapy-Induced Death in Human Hepatoma Carcinoma Huh-7 Cells by Chlorophyll Derivatives
指導教授:李文婷李文婷引用關係
指導教授(外文):Wen-Tyng Li
學位類別:碩士
校院名稱:中原大學
系所名稱:醫學工程研究所
學門:生命科學學門
學類:生物化學學類
論文種類:學術論文
論文出版年:2007
畢業學年度:95
語文別:中文
論文頁數:151
中文關鍵詞:葉綠素衍生物細胞凋亡細胞壞死人類肝癌細胞光動力治療
外文關鍵詞:photodynamic therapyhuman hepatocellular carcinomachlorophyll derivativenecrosisapoptosis
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  • 被引用被引用:7
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光動力療法(Photodynamic therapy,PDT)為癌症患者提供另一創新之醫療概念;其原理是利用光感物質來標定腫瘤細胞,再配合特定波長之光源照射病變組織,進而選擇性的殺死癌細胞。具有不傷害周圍正常組織,以達到治療癌症的優勢。先前本實驗室已證實以菠菜所萃取出之葉綠素衍生物pheophytin a (A3),pheophorbide a (A4)、pheophytin b (B3) 及pheophorbide b(B4)可作為光感物質,導致人類肝癌細胞(HuH-7)死亡,本研究將持續探討PDT對HuH-7導致細胞死亡之作用機制。在研究結果發現四種葉綠素衍生物均會標定於HuH-7細胞之粒線體上,再給予紅光(660 nm)刺激執行PDT後產生大量之ROS,而這些ROS造成HuH-7細胞同時進行凋亡與壞死。針對凋亡之路徑探討結果發現,PDT造成HuH-7細胞的粒腺體膜電位喪失,使Cytochrome c從粒線體釋放至細胞質,Procaspase-9會被活化成Caspase-9,最後再活化Caspase-3。Caspase-3被活化後會將細胞核內的PARP切斷,使PARP失去修復DNA之功能,導致DNA斷裂,造成HuH-7細胞進行凋亡。
Photodynamic therapy (PDT) is an innovative treatment for cancer therapy. The advantage of PDT is specific targeting to the tumor sites without damaging the normal tissue nearby, in which a photosensitizing drug selectively accumulates in tumors and is subsequently activated by visible light of an appropriate wavelength matched to the absorption spectrum of the photosensitizer. Previously we have demonstrated that PDT using chlorophyll derivatives including pheophytin a (A3), pheophytin b (B3), pheophorbide a (A4) and pheophorbide b (B4) has excellent phototoxicity against human hepatocellular carcinoma cells (HuH-7). The objective of the present study was to investigate the mechanism of photodynamic mediated cell death in HuH-7 cells caused by these photosensitizers. Our findings indicated that chlorophyll derivatives could target the mitochondria in HuH-7 cells. With combination of the irradiation of light emitting diodes (LEDs, 660 nm, 10 mW/cm2), the generation of reactive oxygen species and a collapse of mitochondrial membrane potential were observed. The loss of mitochondrial membrane potential led to the release of cytochrome c from the mitochondria to the cytosol, followed by activation of Caspase-9 and Caspase-3. The activation of Caspase-3 resulted in poly(ADP-ribose) polymerase (PARP) cleavage and led to DNA fragmentation in HuH-7 cells. Our results suggest that PDT with chlorophyll derivatives induce apoptosis of HuH-7 cells via the mitochondrial mediated pathway.
中文摘要…………………………………………………………..…..…I
英文摘要…………………………………………………..…………..…II
致謝………………………………………………………..………....…..III
目錄………………………………………………………………………IV
圖索引…………………………………………………….………..…VIII
表索引……………………………………………………….…………...XI
縮寫表…………………………………………………..….…..….…XII
第一章 緒論..............................................................................................1
1-1 前言....................................................................................................1
1-2 文獻回顧............................................................................................2
1-2-1 光動力治療之歷史......................................................................2
1-2-2 光動力治療應用於肝癌..............................................................3
1-2-3 葉綠素衍生物於光動力治療之應用..........................................7
1-3 研究目的與動機................................................................................9
第二章 理論基礎....................................................................................11
2-1 肝癌……………………………………….……………………...11
2-2 光動力治療作用機制……………………………………….…13
2-3 光動力治療要素…………………….…………………….…...15
2-3-1 光源…………………………….……………………………..15
2-3-2 光感藥物………………….……………...…………………….16
2-3-3 氧氣.............................................................................................17
2-4 細胞凋亡…………………………………..……….……………...18
2-4-1 膜受體調控的細胞凋亡………………...……….…………….19
2-4-2 粒線體調控的細胞凋亡……………...…………….………….20
2-5 Caspase……………………………….…..…………….…………..21
2-6 細胞核內的凋亡反應…………………..……………….………...22
第三章 實驗方法與材料……………………..…………………………24
3-1 實驗設計與流程……………………….………………….………24
3-2 實驗設備………………………….……..………………………...25
3-3 實驗藥品…………………………….………..…………………...25
3-4 人類肝癌細胞(HuH-7)培養………….……………..………........26
3-4-1 藥品配置…………………….……….………………………...27
3-4-2 細胞繼代…………………….………...……………………….29
3-5 光動力治療…………………….…………..………………….…30
3-5-1 藥品配置……………………….………...…………………….30
3-5-2 光源………………………….……………...……………….....30
3-5-3 光動力治療步驟……………….………………...…………….32
3-6 實驗方法………………………….……………...……………....32
3-6-1 細胞毒性分析(MTT assay)……….…..…………..……32
3-6-2 觀察光感藥物標定細胞中位置……….……………………35
3-6-3 活性氧分子分析……………….……………………....……36
3-6-4 螢光染色之觀察…………………….……………..…..……39
3-6-5 Annexin V與PI染色.................................................41
3-6-6 Tunel assay-DNA斷裂分析….………..……………….…44
3-6-7 西方點墨法(Western Blot)………..……..……….…...47
第四章 結果....................…………………………….……………...….59
4-1 細胞毒性分析…………………….………………………........….59
4-2 光感藥物標定細胞內之位置……………………..……..……66
4-3 活性氧分子(ROS)分析………………………..……………….…68
4-4 螢光染色觀察……………………………………….………….…71
4-4-1 Hoechst-33258螢光染色…………………..…………..…71
4-4-2 TMRM螢光染色…………….………....…………………74
4-4-3 Rhodamine 123螢光染色….…….…..……………..……76
4-5 Annexin V與PI染色…………..……………...........................….78
4-6 DNA斷裂………………………….......…..…………….………82
4-7 凋亡蛋白之表現…………………………..………....……………85
4-7-1 Cytochrome c釋放………….……............…….………...85
4-7-2 Caspase-9活化………….……………...…….……………89
4-7-3 Caspase-3活化…………..……..……...……………….…96
4-7-4 PAPR斷裂…………....…….……..………………………103
第五章 討論………………….…………..…………..………...………110
5-1 葉綠素衍生物之光動力治療產生之細胞毒性…..….……….....110
5-2 光感物質累積之位置……….……………………..…………….111
5-3 葉綠素衍生物之光動力治療產生之活性氧分子……...………..112
5-4 葉綠素衍生物之光動力治療產生之粒腺體膜電位變化情形….112
5-5 葉綠素衍生物之光動力治療產生之凋亡路徑探討……...……..113
5-6 葉綠素衍生物之光動力治療產生之凋亡特性表現……...……..115
第六章 結論與未來展望………………………………...…..…………117
參考文獻…………………………………………………...…………120
附錄圖………………………………………………..…...…………….126
附錄表………………………………………………..…...…………….134

表索引
表1-1光動力治療應用於肝癌文獻回顧………….……….…………6
表1-2葉綠素衍生物於光動力治療相關文獻回顧.……….………….9
表3-1人類肝癌細胞株資料表….……………………………………27
表3-2細胞毒性測試之光感藥物濃度表……………………………33
表3-3 Homo-buffer藥物劑量表…………………..…………………48
表3-4 4X SDS 樣本液之藥物劑量表………………………………49
表3-5電泳液藥物劑量表……………………………………………50
表3-6 TBST溶液藥物劑量..………………….……………………50
表3-7 AP buffer藥物劑量表…………...…………………………51
表3-8 Stripping buffer藥物劑量表……..……….…….…....………51
表3-9 蛋白質分子量與其抗體特性表…….………………..…...…55
表3-10 SDS-PAGE 膠體配置藥品劑量表…….………………………56
附 表 A 實驗設備表………………………………………………….134
附 表 B 實驗藥品表………………………………………………….136

圖索引
圖3-1 人類肝癌細胞株(HuH-7)之細胞型態圖…...…………26
圖3-2 實驗光源-660 nm發光二極體…………...……….……31
圖3-3 轉印夾裝置示意圖………….……………………….……57
圖4-1 葉綠素衍生物-pheophytin a(A3)對HuH-7之細胞毒性
分析…………………………………………………………...62
圖4-2 葉綠素衍生物-pheophytin b(B3)對HuH-7之細胞毒性
分析 …………………………………………..……………..63
圖4-3 葉綠素衍生物-pheophorbide a(A4)對HuH-7之細胞毒性
分析…………………………………………..……………64
圖4-4 葉綠素衍生物-pheophorbide b(B4)對HuH-7之細胞毒性
分析………………………………………….……………...65
圖4-5 葉綠素衍生物於標定細胞內之位置之情形…………..…67
圖4-6 光動力治療後對HuH-7細胞內之活性氧分子含量分析.70
圖4-7 Hoechst 33258染色之結果………………………...…73
圖4-8 TMRM染色之結果…………………..……………...…75
圖4-9 Rhodamine 123染色結果圖…………..…………...…77
圖4-10 Annexin V與PI染色情形………….…………………..80
圖4-11 Annexin V與PI之定量分析……….…………………..81
圖4-12 凋亡細胞與壞死細胞之定量比較圖……….…………...82
圖4-13 光動力治療後以Tunel分析HuH-7細胞之DNA斷裂
情形………………………………………………………..….85
圖4-14 光動力治療後造成 HuH-7 之 Cytochrome c 釋放情形與影像分析結果…………………………….……………………..88
圖4-15 光動力治療後造成 HuH-7 之 Caspase-9 活化情形與影像分析之結果……………………………….……………………..95
圖4-16 光動力治療後造成 HuH-7 之 Caspase-3 活化情形與影像分析之結果……………………………….………..…………..102
圖 4-17 光動力治療後造成 HuH-7之 PARP 斷裂情形與影像分析之結果……………………………………………………….109
圖6-1 光動力治療造成肝癌細胞死亡之機制圖…………….119
附 圖 A 台灣地區歷年之肝癌死亡率……….…………………….126
附 圖 B 光動力治療之機制圖……………….………………….....127
附 圖 C 細胞壞死與細胞凋亡…………….……………...……..128
附 圖 D 細胞凋亡調控機制圖…………….………………….....129
附 圖 E 膜受體調控的細胞凋亡路徑…….……………………..130
附 圖 F 粒線體調控的細胞凋亡路徑…….……………………..131
附 圖 G Caspase 蛋白質之結構……….……………………...132
附 圖 H Caspase在細胞核內引發之凋亡作用機制.…………….133
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