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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 劉興華 | |
| dc.contributor.author | Chia-Wei Kao | en |
| dc.contributor.author | 高佳薇 | zh_TW |
| dc.date.accessioned | 2021-06-07T18:03:53Z | - |
| dc.date.copyright | 2012-09-19 | |
| dc.date.issued | 2012 | |
| dc.date.submitted | 2012-07-30 | |
| dc.identifier.citation | Aird WC (2007a) Phenotypic heterogeneity of the endothelium: I. Structure, function, and mechanisms. Circulation Research 100: 158-173
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/16175 | - |
| dc.description.abstract | 糖尿病為慢性代謝異常疾病，主因為體內的胰島素分泌不足或胰島素阻抗導致體內高血糖現象。而高血糖是引發糖尿病血管併發症的原發因子，往往影響患者的生活品質並導致患者壽命減短。血管內皮功能受損被認為是糖尿病血管病變的重要致病機轉，許多研究指出，內皮細胞的凋亡導致早期糖尿病小血管病變的發生。糖化終產物，是由糖與蛋白質分子相互聚合經過一系列的反應後產生的不可還原之物質。糖尿病患者體內高血糖狀況引發糖化終產物的生成及累積，與糖尿病血管病變的進展有關。許多先前研究已證實糖化終產物會引起多種細胞的凋亡，然而其影響胰島內皮細胞之作用，尚未明瞭。因此，本篇研究利用胰島內皮細胞株 (MS1細胞)，探討糖化終產物誘發胰島內皮細胞凋亡之作用機制。實驗結果得出，給予MS1細胞處理糖化終產物200 μg/ml 24小時後，細胞內磷酸化P65、環氧化酵素、cleaved caspase-3及cleaved PARP的蛋白表現增加，而細胞存活率減少24.1%，並且有MS1細胞凋亡現象。予以前處理環氧化酵素的抑制劑，抑制環氧化酵素活性，以降低前列腺素E2的產生後，糖化終產物引發之cleaved caspase-3及cleaved PARP的蛋白表現則隨之減少，並回復MS1細胞之存活率 (由70.3%回復至78.8%)。此實驗結果顯示，糖化終產物引發之胰島內皮細胞凋亡現象涉及環氧化酵素的活性激發，在糖尿病患者胰島之病變上可能扮演著一個重要的角色。 | zh_TW |
| dc.description.abstract | Diabetes mellitus (DM), a metabolic disorder, is characterized by hyperglycemia and insulin resistance. Hyperglycemia has been shown to be responsible for the development and progression of diabetic vasculopathy, which result in shortened life expectancy, increased morbidity and diminished quality of life in DM patients. Endothelium dysfunction is an important pathophysiological factor in diabetic vasculopathy. Previous studies have indicated that endothelial cell apoptosis plays an important role in the development of early lesions in DM micro vasculopathy. Advanced glycation end-products (AGEs), which form and accumulate under hyperglycemia of diabetes, are implicated in the progression of diabetic vascular complications. Several studies have demonstrated that AGEs can triggered apoptosis in various kind of cells. However, there is no similar evidence in the islet-derived endothelial cells. In the present study, pancreatic islet endothelial cells (MS1 cell line) were used to investigate the cytotoxicity of AGEs. The results showed that AGEs induced P65 phosphorylation, COX-2 activation, expression of cleaved caspase-3 and cleaved PARP, reduced 24.1% cell viability, and led to cell apoptosis. Pretreatment with NS398 (COX-2 inhibitor) to inhibit PGE2 production reversed the induction of cleaved caspase-3 and cleaved PARP and MS1 cell viability. In conclusion, the experimental results provide an insight into the pathological processes taking place within the pancreatic islet endothelium caused by AGEs and suggest that induction of COX-2 activation may play an important role in the pathogenesis of islets in diabetes. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-07T18:03:53Z (GMT). No. of bitstreams: 1 ntu-101-R99447003-1.pdf: 2171617 bytes, checksum: ed8d3e3f8b6b39baf5a6bbf18b7a729f (MD5) Previous issue date: 2012 | en |
| dc.description.tableofcontents | Contents…………………………………………………………………..…………….i
中文摘要…………………………………………………….…………..……...……..iii Abstract……………………………………………………………………..…………iv Abbreviations………………………………………………….…………….………..vi CHAPTER I Introduction……………………………………….……..…………1-16 1. Diabetes mellitus (DM)…………..........……………………………..…….....1 2. Vascular complications in diabetes…..………………...……………..………...3 3. Advanced glycation end-products (AGEs)……………………………..….…10 4. Aims……………………………………………...……………..………..……16 CHAPTER II Materials and Methods…………………………..…...…...….….17-22 CHAPTER III Results…………………………………...…..……………...……23-25 1. AGEs influenced the progression of diabetes……………………….……..….23 2. AGEs reduced MS1 cell viability…………………………..……...…...…..….23 3. AGEs induced apoptosis in MS1 cells………………...………………….....…24 4. ER stress did not involve in AGEs-induced MS1 cell apoptosis…................…24 5. Exposure to AGEs increased protein expression of p-P65 and COX-2………..24 6. COX-2 mediated AGEs-induced MS1 cell apoptosis……………………….…25 CHAPTER IV Discussion…………………………..……………..……….…….26-29 Figures…………………………………………….………………….……..…….30-40 Supplementary Figures…………….…………………….………….……..………..41 References…………………………………….……………………………..…….42-48 | |
| dc.language.iso | en | |
| dc.title | 糖化終產物引發胰島內皮細胞凋亡之機制探討 | zh_TW |
| dc.title | The mechanism of advanced glycation end-products on apoptosis of pancreatic islet endothelial cells | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 100-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 蕭水銀,楊榮森,姜至剛,陳敞牧 | |
| dc.subject.keyword | 糖化終產物,細胞凋亡,胰臟胰島內皮細胞, | zh_TW |
| dc.subject.keyword | Advanced glycation end-products (AGEs),cell apoptosis,pancreatic islet endothelial cells, | en |
| dc.relation.page | 48 | |
| dc.rights.note | 未授權 | |
| dc.date.accepted | 2012-07-31 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 毒理學研究所 | zh_TW |
| 顯示於系所單位： | 毒理學研究所 | |
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