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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 郭彥彬 | |
| dc.contributor.author | Hsi-Wen Wang | en |
| dc.contributor.author | 王希文 | zh_TW |
| dc.date.accessioned | 2021-06-15T01:20:42Z | - |
| dc.date.available | 2014-09-15 | |
| dc.date.copyright | 2009-09-15 | |
| dc.date.issued | 2009 | |
| dc.date.submitted | 2009-07-27 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/42716 | - |
| dc.description.abstract | 根據行政院衛生署統計民國96年國人十大死因，心臟疾病與腦血管疾病分別位居第二及第三名，嚴重威脅國人健康。近年研究顯示細菌感染可能是血管發生病變的原因之一，其中牙周病亦與心血管疾病具密切相關性。 Porphyromonas gingivalis (P.g.)是造成牙周病的致病菌之一，文獻指出P.g.會隨血液在血管裡流動，出現在動脈硬化發生的區域。 最近研究發現，粥狀動脈硬化斑塊處有大量的Cyr61及Egr-1表現。Cyr61表現量的多寡與動脈硬化惡化程度呈正比，Cyr61及Egr-1 刪除鼠可以抑制粥狀動脈硬化動物模式的粥狀動脈硬化發生。 本研究探討P.g. 誘導Cyr61及Egr-1表現產生動脈硬化的可能性。 我們首先以1ug/ml P.g. 脂多醣( LPS)處理人類血管平滑肌細胞(VSMC) ，發現LPS會誘導Cyr61及Egr-1的蛋白與mRNA表現。在VSMC中ROS並非Cyr61及Egr-1的誘導來源，但利用Bay (NF-kB抑制劑)、PD98059、SP600125、SB203580(ERK、JNK、p38抑制劑) 及Epigallocatechin gallate (EGCG)前處理可阻斷P.g. LPS誘導的Cyr61蛋白表現。可見得MAPKs訊息傳遞路徑在VSMC誘導的Cyr61蛋白表現中扮演了重要活化角色。然而由P.g. LPS誘導的Egr-1蛋白表現只受到SP600125及curcumin (AP-1抑制劑)的抑制。在粥狀動脈硬化微環境中有大量吞噬細胞存在，因此我們以1ug/ml P.g. LPS處理人類單核球細胞株THP-1亦發現它會誘導Cyr61及Egr-1的蛋白與mRNA表現。以PD98059、SP600125、Bay、抗氧化劑N- acetylcysteine及EGCG前處理可阻斷LPS誘導的Cyr61蛋白表現。在Egr-1蛋白的部分與VSMC結果相同，Egr-1蛋白表現只受到SP600125及curcumin的抑制。本研究首次指出P.g. LPS可誘導血管平滑肌細胞及人類單核球細胞 Cyr61及Egr-1蛋白之表現。 其訊息傳遞路徑可能經由ROS及MAPKs路徑。冀望未來可以藉由抑制這些訊息傳遞路徑成員來抑制與牙周病相關的動脈硬化。 | zh_TW |
| dc.description.abstract | According to the 2007 census of department of health, Executive Yuan, ROC, heart disease and cerebral vascular disease rank second and third among ten leading causes of death, respectively. Epidemiological studies have shown that periodontal disease is associated with increased risk for cardiovascular and cerebrovascular disease. With Porphyromonas gingivalis (P.g.) as the most important periodontal pathogen, this organism can accelerate atheroma deposition in animal models. However, the detail mechanism remains unknown. Previous studies have shown that Cyr61 and Egr-1 are highly expressed in human atherosclerotic plaques, correlating with the degree of stenosis and plaque histopathology. Inhibition of Cyr61 and Egr-1 gene expression reduces neointimal hyperplasia following balloon injury in rats. Here we show 1μg/ml P. g. LPS markedly induces Cyr61 and Egr-1 in mRNA and protein level in human vascular smooth muscle cell (VSMC) and human monocytic THP-1 cells. Pretreatment with NF-kB inhibitor Bay 11-7082, ERK inhibitor PD98059, JNK inhibitor SP600125, p38 MAPK inhibitor SB203580 and antioxidant epigallocatechin gallate (EGCG) significantly reduced P. g. LPS-induced Cyr61 in human vascular smooth muscle cells (VSMC), whereas the induction of Egr-1 via P. g. LPS only affected by SP600125 and curcumin (AP-1 inhibitor). In THP-1 cells, pretreatment with ROS inhibitor NAC, Bay 11-7082, PD98059, SP600125 and EGCG significantly reduced P. g. LPS-induced Cyr61, but not SB203580. The induction of Egr-1 by P. g. LPS in THP-1 also affected by SP600125 and curcumin. In conclusion, our results provide the first evidence that chronic P.g. infection may contribute to atherogenesis through sustained upregulation of Cyr61 and Egr-1. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T01:20:42Z (GMT). No. of bitstreams: 1 ntu-98-R96450002-1.pdf: 2131657 bytes, checksum: 5fbbcf99419f7e01651198bc37a22bcc (MD5) Previous issue date: 2009 | en |
| dc.description.tableofcontents | 中文摘要 1
Abstract 2 導論 3 第一節 牙周病(Periodontal Disease) 3 1-1 牙周病 3 1-2 牙周病的致病原因- 牙菌斑 3 1-3牙周病與口腔細菌及其致病機轉 4 第二節 動脈硬化(Atherosclerosis) 6 2-1動脈硬化流病學 6 2-2動脈硬化病理學 6 動脈硬化發生機轉 6 2-3動脈硬化的危險因子 8 2-4牙周病與心血管疾病相關性之流行病學證據 8 2-5牙周致病菌對心臟血管疾病之致病機轉 9 2-6牙周病、發炎和心血管疾病之間的關係 10 2-7 P. gingivalis與動脈硬化的關係 11 2-8脂多醣(lipopolysaccharide; LPS) 11 2-9氧化壓力(ROS)與動脈硬化 12 Mitogen-activated protein kinases 路徑 13 第三節 Cyr61(Cysteine-rich protein) 14 3-1 Cyr61的簡介 14 3-2 Cyr61與動脈硬化的關係 15 3-3 Cyr61訊息傳遞路徑及基因調控 15 第四節 Egr-1(Early Growth Response-1) 16 4-1 Egr-1的簡介 16 4-2 Egr-1與動脈硬化的關係 16 4-3 Egr-1訊息傳遞路徑及基因調控 17 實驗目的 18 實驗材料與方法 19 第一節 細胞株與細胞培養 19 第二節 藥物的處理 19 第三節 西方墨點法 20 第四節 RNA的萃取 23 第五節 RNA的反轉錄 23 第六節Real-Time PCR 24 第七節 利用Flow cytometry作活性氧自由基的測定 25 結果 26 P. gingivalis LPS會誘導人類血管平滑肌細胞VSMC中Cyr61及Egr-1 mRNA的表現…………………………………………………………………………..26 P. gingivalis LPS會誘導VSMC細胞中Cyr61及Egr-1蛋白的表現 26 MAPKs抑制劑可抑制VSMC細胞由P. gingivalis LPS所誘導的Cyr61及Egr-1 27 P. gingivalis LPS誘導VSMC細胞中Cyr61及Egr-1蛋白表現的訊息傳導路徑 27 P. gingivalis LPS會促進VSMC細胞中p38 MAPK、JNK及ERK磷酸化 28 P. gingivalis LPS會誘導人類單核球細胞株THP-1中Cyr61及Egr-1蛋白的表現 28 P. gingivalis LPS會誘導THP-1細胞株中Cyr61及Egr-1 mRNA表現 29 P. gingivalis LPS誘導THP-1細胞株中Cyr61及Egr-1蛋白表現的訊息傳導路徑 29 P. gingivalis LPS會促進THP-1細胞株中ERK及JNK磷酸化 30 NAC可抑制THP-1細胞株由P. gingivalis LPS所誘導的ERK及JNK 磷酸化 31 P. gingivalis LPS可誘導THP-1細胞株產生ROS 31 討論 33 圖 37 圖一、P.g. LPS會誘導VSMC細胞中Cyr61及Egr-1 mRNA 的表現 37 圖二、P.g. LPS誘導VSMC細胞Cyr61及Egr-1 表現的情形 38 圖三、在VSMC細胞中P.g. LPS對於Cyr61及Egr-1的誘導受到MAPKs的調控 39 圖四、LPS誘導VSMC細胞中Cyr61及Egr-1蛋白表現的訊息傳導路徑 40 圖五、在VSMC細胞中加入P.g. LPS會誘導p38、JNK及ERK的磷酸化 41 圖六、P.g. LPS誘導THP-1細胞Cyr61及Egr-1 表現的情形 42 圖七、P.g. LPS會誘導THP-1細胞中Cyr61及Egr-1 mRNA 的表現 43 圖八、P.g. LPS誘導THP-1細胞中Cyr61蛋白表現的訊息傳導路徑 44 圖九、P.g. LPS誘導THP-1細胞中Egr-1蛋白表現的訊息傳導路徑 45 圖十、P.g. LPS會促進THP-1細胞中ERK及JNK磷酸化 46 圖十一、在THP-1細胞中， P.g. LPS可能藉由刺激細胞產生ROS來活化ERK及JNK的表現 47 圖十二、P.g. LPS刺激THP-1細胞產生ROS 48 參考文獻 61 | |
| dc.language.iso | zh-TW | |
| dc.title | 牙周致病菌 porphyromonas gingivalis在動脈硬化中誘導細胞表現Egr-1及Cyr61之機轉 | zh_TW |
| dc.title | Porphyromonas gingivalis induces vascular cells expression of Egr-1 and Cyr61 in atherosclerosis | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 97-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 劉謙美,呂炫? | |
| dc.subject.keyword | Porphyromonas gingivalis,動脈硬化,Cyr61,Egr-1, | zh_TW |
| dc.subject.keyword | Porphyromonas gingivalis,atherosclerosis,Cyr61,Egr-1, | en |
| dc.relation.page | 66 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2009-07-27 | |
| dc.contributor.author-college | 牙醫專業學院 | zh_TW |
| dc.contributor.author-dept | 口腔生物科學研究所 | zh_TW |
| 顯示於系所單位： | 口腔生物科學研究所 | |
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| ntu-98-1.pdf 目前未授權公開取用 | 2.08 MB | Adobe PDF |
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