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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 邱智賢 | zh_TW |
| dc.contributor.advisor | Chih-Hsien Chiu | en |
| dc.contributor.author | 江紀明 | zh_TW |
| dc.contributor.author | Chi-Ming Chiang | en |
| dc.date.accessioned | 2024-01-26T16:36:46Z | - |
| dc.date.available | 2024-01-27 | - |
| dc.date.copyright | 2024-01-26 | - |
| dc.date.issued | 2024 | - |
| dc.date.submitted | 2024-01-22 | - |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/91462 | - |
| dc.description.abstract | 臨床上，如果肝臟受到慢性損傷，諸如酒精傷害、感染病毒、或藥物影響，將導致骨量減少。研究指出，近20%慢性病毒性肝炎患者有骨質疏鬆或是骨質減少的情形。尤其是患有慢性膽囊炎的患者，超過60%出現骨量減少的問題；而患有酒精性或病毒性肝硬化的患者，出現發生骨質疏鬆症的機率甚至高達90%以上。
生理學上IGF-1對於骨骼的生展發育至關重要，它主要由肝臟分泌，可以刺激骨原細胞成為成骨細胞，進而增加成骨細胞的總量。此外，IGF-1還能抑制骨的吸收，降低骨中的膠原蛋白被分解，有助於維持骨量。因此，當體內IGF-1的水平下降，可能會影響骨量，從而導致骨質疏鬆或其他相關的骨骼問題。 本研究先從臨床的觀點出發，探討肝性骨病變與肝骨軸的相互影響。根據內分泌體介導素假說(somatomedin hypothesis)，當肝硬化發生時，可以推斷由肝臟生產的IGF-1水平會降低，而IGF-1負責調控骨細胞數量。然而，VitD3為固醇類類似物，所以使用VitD3治療又為避免發炎而輔以Dexthamethasome(Dex)成功將患者治癒。其次，動物模型實驗結果顯示，在四氯化碳誘導的肝性骨病變大鼠中，IGF-1並不影響大鼠間質幹細胞的增殖或分化。這一發現引起了對肝骨軸機制的重新評估， IGF-1或許不是調控分化間質幹細胞的關鍵。此外，以MTT assay和real-time PCR(q PCR)技術，分析人類成骨細胞（hFOB 1.19）和小鼠成骨細胞（7F2）的增生能力及mRNA基因表現量，顯示Vit D3和低劑量Dexamethasone顯著提升成骨細胞的增殖和形成骨礦化，且低劑量類固醇能顯著上調IGF-1受體表現量，將使更多的IGF-1受體接收IGF-1，克服肝性骨病變患者胰臟分泌IGF-1不足之困境。 此研究成果對於臨床治療有著極其重要的意義。首先，推翻過去臨床長期使用Dexamethasone造成骨鬆之顧慮，低劑量Dexamethasone反而對成骨細胞增生與礦化有益，低劑量類固醇的使用可能成為一種有潛力的治療策略。 其次，由於Vit D3為脂溶性維生素，代謝不易，臨床治療需密切監控體內血鈣濃度，防止血鈣中毒。因此本研究提供以Dexamethasone取代Vit D3的治療方案。 最後Dexamethasone上調IGFR總表現量，在肝骨軸路徑可使肝性骨病變患者，肝臟分泌之IGF接收更為全面，反證IGF-1在肝骨軸協同骨癒合極具重要性。本研究為肝性骨病變之治癒提供了一個全面而深入的框架，這將有助於進一步解析肝性骨病變和相關疾病的複雜機制。 | zh_TW |
| dc.description.abstract | This study focuses on exploring the interplay between hepatic bone disease and the liver-bone axis. According to the somatomedin hypothesis, cirrhosis may lead to a decrease in liver-produced IGF-1 levels. However, the study found that treatment with VitD3 (a form of Vitamin D3) and low-dose Dexamethasone (a steroid medication) effectively combats hepatic bone disease. Notably, low-dose Dexamethasone significantly enhances the proliferation and mineralization of osteoblasts and upregulates the expression of IGF-1 receptors, overcoming the deficiency in liver-secreted IGF-1.
These findings have significant implications for clinical treatment. They indicate that low-dose Dexamethasone not only does not lead to osteoporosis but actually benefits the proliferation and mineralization of osteoblasts. Additionally, considering the lipophilic nature and metabolic characteristics of Vit D3, it is crucial in clinical treatments to closely monitor blood calcium levels to prevent hypercalcemia. Therefore, replacing Vit D3 with Dexamethasone might be an effective treatment strategy. Moreover, the role of Dexamethasome in upregulating the total expression of IGFR (IGF-1 receptor) highlights the importance of IGF-1 in the liver-bone axis for bone healing. Overall, this study provides a comprehensive and in-depth framework for the treatment of hepatic bone disease, which will aid in further unraveling the complex mechanisms of hepatic bone disease and related disorders. | en |
| dc.description.provenance | Submitted by admin ntu (admin@lib.ntu.edu.tw) on 2024-01-26T16:36:46Z No. of bitstreams: 0 | en |
| dc.description.provenance | Made available in DSpace on 2024-01-26T16:36:46Z (GMT). No. of bitstreams: 0 | en |
| dc.description.tableofcontents | 口試委員會審定書 i
謝 辭 ii 中文摘要 iv Abstract vi 目次 viii 圖次 x 表次 xii 第一章 序 論 1 1.1 肝骨軸的生理學基礎 1 第二章 文獻回顧 6 2.1 肝硬化與骨代謝障礙 6 2.2 肝性骨病變 7 2.3 類胰島素生長因子（Insulin Like Growth Factor 1, IGF-1） 11 2.4 IGF結合蛋白（Insulin Like Growth Factor binding protein） 13 2.5 生長激素與類胰島素生長因子軸GH/IGF-1 axis 16 2.6 內分泌體介素假說Somatomedin Hypothesis 19 第三章 研究材料與方法 21 3.1 肝性骨病變的動物建模與骨髓MSC與HSC的比較 21 3.1.1肝性骨病變之臨床案例 21 3.1.2肝性骨病變的動物建模 29 （1）建立實驗主體 29 （2）設定實驗的週期 29 （3）骨髓細胞檢體製備 30 （4） 運用Hematoxylin & Eosin（H&E）染色技術 30 3.1.3 骨髓濃縮物萃取分析 31 3.2 肝骨軸的細胞學實驗 32 3.2.1研究目的 32 3.2.2 研究材料 33 （1）細胞樣本 33 （2）培養基成分 33 3.2.3 研究方法 34 （1） MTT assay 34 （2）即時量化聚合酶鏈反應(Real-time Quantitative Polymerase. Chain Reaction， q-PCR ) 34 （3）西方墨點（Western Blot） 39 第四章 結 果 42 4.1 模式動物結果 42 4.1.1 肝性骨病變建模完成 42 4.1.2 濃縮骨髓萃取物的流式細胞儀分析結果 42 4.2 細胞學實驗結果 43 4.2.1透過MTT assay了解成骨細胞的活性 43 4.2.2量化聚合酶鏈反應解釋肝骨軸的作用與機制 44 4.2.3西方墨點（Western Blot） 46 4.3 肝骨軸的細胞學原理 46 4.3.1 類固醇與維他命D3對細胞的關聯性 46 4.3.2 Ki-67和PCNA兩種物質可能促進細胞增殖 47 4.3.3 類固醇受體以及維他命D受體促進骨形成和代謝過程 47 4.3.4 類固醇在骨代謝中的作用具有重要意義 48 4.3.5 低劑量類固醇對成骨細胞中膠原蛋白I（collagen I）和骨鈣蛋白（osteocalcin）基因表達顯著增加。 48 4.3.6 低劑量類固醇能夠促進成骨細胞的增殖 49 4.3.7 低劑量類固醇顯著增加了膠原蛋白I（collagen I）和骨鈣蛋白（osteocalcin）的蛋白質 49 第五章 討論 78 5.1 四氯化碳誘導肝性骨病變大鼠模型中骨髓幹細胞的流式細胞儀分析 78 5.2 IGF-I(Insulin-like growth factor 1) 與(Mesenchymal Stem Cells, MSCs) 78 5.3 內分泌體介素假說的疑問 81 5.4 糖皮質激素與糖皮質激素受體 83 5.5低劑量類固醇與IGF-1信號傳遞 85 第六章 結 論 90 參考資料 97 | - |
| dc.language.iso | zh_TW | - |
| dc.title | 肝性骨病變之肝骨軸研究 | zh_TW |
| dc.title | Study on the Liver-Bone Axis of Hepatic Osteodystrophy | en |
| dc.type | Thesis | - |
| dc.date.schoolyear | 112-1 | - |
| dc.description.degree | 博士 | - |
| dc.contributor.oralexamcommittee | 張振慧;陳億乘;黃啟彰;徐慶琳 | zh_TW |
| dc.contributor.oralexamcommittee | Jen-huei Chang;Yi-Cheng Chen;Chi-Chang Huang;Chin-Lin Hsu | en |
| dc.subject.keyword | 糖皮質激素受體,維他命D,維他命D受體,Wnts訊號,肝骨軸,內分泌體介導素假說, | zh_TW |
| dc.subject.keyword | Glucocorticoid Receptor,Vitamin D,Vitamin D Receptor,Wnt Signaling,Liver-Bone Axis,Somatomedin Hypothesis, | en |
| dc.relation.page | 112 | - |
| dc.identifier.doi | 10.6342/NTU202400138 | - |
| dc.rights.note | 同意授權(全球公開) | - |
| dc.date.accepted | 2024-01-23 | - |
| dc.contributor.author-college | 生物資源暨農學院 | - |
| dc.contributor.author-dept | 動物科學技術學系 | - |
| 顯示於系所單位： | 動物科學技術學系 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-112-1.pdf | 4.77 MB | Adobe PDF | 檢視/開啟 |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。