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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/84961完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 林璧鳳(Bi-Fong Lin) | |
| dc.contributor.author | Li-Fen Chen | en |
| dc.contributor.author | 陳立芬 | zh_TW |
| dc.date.accessioned | 2023-03-19T22:35:05Z | - |
| dc.date.copyright | 2022-08-26 | |
| dc.date.issued | 2022 | |
| dc.date.submitted | 2022-08-23 | |
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(2021); 45(1):11-26. doi: 10.4093/dmj.2020.0217. Yan LJ. Folic acid-induced animal model of kidney disease. Animal Model Exp Med. (2021); 4(4):329-342. doi: 10.1002/ame2.12194. Zhang J, Jiang T, Liang X, Shu S, Xiang X, Zhang W, Guo T, Xie W, Deng W, Tang X. lncRNA MALAT1 mediated high glucose-induced HK-2 cell epithelial-to-mesenchymal transition and injury. J Physiol Biochem. (2019); 75(4):443-452. doi: 10.1007/s13105-019-00688-2. Zhang R, Ma J, Xia M, Zhu H, Ling W. Mild hyperhomocysteinemia induced by feeding rats diets rich in methionine or deficient in folate promotes early atherosclerotic inflammatory processes. J Nutr. (2004); 134(4):825-30. doi: 10.1093/jn/134.4.825. Zhang T, Li H, Shi J, Li S, Li M, Zhang L, Zheng L, Zheng D, Tang F, Zhang X, Zhang F, You X. p53 predominantly regulates IL-6 production and suppresses synovial inflammation in fibroblast-like synoviocytes and adjuvant-induced arthritis. Arthritis Res Ther. (2016); 18(1):271. doi: 10.1186/s13075-016-1161-4. Zhao R, Matherly LH, Goldman ID. Membrane transporters and folate homeostasis: intestinal absorption and transport into systemic compartments and tissues. Expert Rev Mol Med. (2009); 11:e4. doi: 10.1017/S1462399409000969. Zhou J, Zhang S, Sun X, Lou Y, Yu J. Hyperoside Protects HK-2 Cells Against High Glucose-Induced Apoptosis and Inflammation via the miR-499a-5p/NRIP1 Pathway. Pathol Oncol Res. (2021); 27:629829. doi: 10.3389/pore.2021.629829. Zhou L, Xu DY, Sha WG, Shen L, Lu GY, Yin X, Wang MJ. High glucose induces renal tubular epithelial injury via Sirt1/NF-kappaB/microR-29/Keap1 signal pathway. J Transl Med. (2015); 13:352. doi: 10.1186/s12967-015-0710-y. Zhu Y, Cui H, Xia Y, Gan H. RIPK3-Mediated Necroptosis and Apoptosis Contributes to Renal Tubular Cell Progressive Loss and Chronic Kidney Disease Progression in Rats. PLoS One. (2016); 11(6):e0156729. doi: 10.1371/journal.pone.0156729. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/84961 | - |
| dc.description.abstract | 糖尿病腎病變是糖尿病的嚴重併發症，也是導致末期腎臟病最主要原因。現 代化飲食易引起肥胖及葉酸營養不足，近年研究觀察到葉酸不足會增加慢性腎臟 病的風險，因此，葉酸與腎臟疾病的關係值得探討。已知高葡萄糖與果糖皆會誘 導腎細胞發炎與纖維化，進而導致腎損傷，而本研究室先前也觀察到葉酸缺乏會 加劇高豬油高果糖飲食小鼠的腎炎與纖維化，但高糖與葉酸對於腎細胞的影響尚 不清楚，故本研究欲使用近端腎小管上皮細胞株 HK-2 細胞，探討葉酸營養狀況 與高糖對腎細胞分泌促發炎和纖維化因子的影響。將 HK-2 細胞培養於不同濃度 葡萄糖或果糖，結果發現葡萄糖或果糖會增加 HK-2 細胞分泌 IL-6、MCP-1 與 TGF-β1。低濃度 LPS 與葡萄糖共同刺激增加 MCP-1，而高濃度 LPS 與葡萄糖或 果糖共同刺激則增加 IL-6 與 TGF-β1。瘦體素與葡萄糖共同刺激 HK-2 細胞增加 IL-6、MCP-1 與 TGF-β1，瘦體素與果糖共同刺激則增加 IL-6。以葡萄糖或果糖刺 激 HK-2 細胞皆導致 p53 基因表現量顯著增加，表示葡萄糖或果糖會增加細胞凋亡 基因表現。此外，以不同葉酸濃度 (f0、f1 與 f5) 培養 HK-2 細胞，發現 f0 顯著降 低 IL-6，但增加 MCP-1 與 TGF-β1。不同葉酸與高糖培養下，f0 降低葡萄糖刺激 的 IL-6，但增加 MCP-1 與 TGF-β1，而 f5 則降低葡萄糖或果糖刺激所分泌的 MCP- 1。最後，不同葉酸濃度培養下，f0 顯著增加 kim-1、 p53 與 caspase-3 基因表現。 總結，葡萄糖與果糖加劇 LPS 或瘦體素刺激下腎細胞分泌促發炎與纖維化因子， 也會增加細胞凋亡基因表現。葉酸缺乏加劇腎細胞在高葡萄糖與果糖下 MCP-1 與 TGF-β1 的分泌，補充葉酸則降低 MCP-1 的分泌。缺葉酸也顯著增加腎損傷與細 胞凋亡相關基因，顯示葉酸缺乏可能為促進腎臟疾病的危險因子。 | zh_TW |
| dc.description.abstract | Diabetic kidney disease is the major cause of end-stage kidney disease. Modern diets are closely associated with the development of obesity and folate deficiency. Previous studies have shown that low folate levels showed a significant association with the higher risk of chronic kidney disease. However, whether folate deficiency and high sugar could result in renal inflammation and fibrosis is still unclear. The aim of this study was to investigate the effects of folate and sugar on the proinflammatory and fibrotic factors by using renal tube cell line (HK-2). HK-2 cells were cultured in different concentrations of glucose or fructose. The results demonstrated that glucose or fructose had a concentration- dependent effect on the secretion of IL-6, MCP-1 and TGF-β1. Co-stimulation of low concentrations of LPS with glucose increased MCP-1, while co-stimulation of high concentrations of LPS with glucose or fructose increased IL-6 and TGF-β1.Further, co- stimulation of leptin and glucose increased IL-6, MCP-1 and TGF-β1 in HK-2 cells, and co-stimulation of leptin and fructose increased IL-6. Stimulation of HK-2 cells with glucose or fructose resulted in a significant increase in p53 gene expression. In addition, HK-2 cells were cultured with different folate medium (f0, f1, and f5). f0 was found to significantly reduce IL-6, but increase MCP-1 and TGF-β1. Under different folate status and high sugar cultures, f0 decreased glucose-stimulated IL-6, but increased MCP-1 and TGF-β1, while f5 decreased glucose- or fructose-stimulated MCP-1 secretion. Finally, f0 significantly increased the expression of kim-1, p53 and caspase-3 genes. In conclusion, high sugar increased proinflammatory and fibrotic cytokines from HK-2 cells stimulated by LPS or leptin. Folate deficiency aggravates the secretion of MCP-1 and TGF-β1 from HK-2 cells under high sugar status, while supplementation of folate reduces MCP-1. Folate deficiency also increases genes related to renal injury and apoptosis, and thus, inadequate folate status might be one of the risk factors for kidney disease. | en |
| dc.description.provenance | Made available in DSpace on 2023-03-19T22:35:05Z (GMT). No. of bitstreams: 1 U0001-1708202215074100.pdf: 4171598 bytes, checksum: 9e8b12b84245e0c472dc3687e09fc8c2 (MD5) Previous issue date: 2022 | en |
| dc.description.tableofcontents | 口試委員會審定書 i 謝誌 ii 摘要 iii Abstract iv 目錄 v 圖目錄 viii 表目錄 ix 縮寫對照表 x 第一章 文獻回顧 1 第一節 葉酸 1 一、葉酸簡介 1 二、葉酸的生理功能 2 三、葉酸與疾病 3 四、葉酸與發炎反應 4 第二節 腎臟 5 一、腎臟構造與功能 5 二、腎臟疾病 7 三、腎臟疾病與發炎反應 9 四、腎臟疾病相關細胞激素 9 1. IL-6 10 2. MCP-1 11 3. TGF-β 11 五、腎臟疾病與葉酸 12 第三節 亮細胞腎癌 13 第四節 糖尿病腎病變 14 一、簡介 14 二、糖尿病腎病變與高葡萄糖 14 三、糖尿病腎病變與高果糖 15 四、糖尿病腎病變與KIM-1 16 五、糖尿病腎病變與細胞凋亡 16 第五節 HK-2細胞株 17 第二章 探討葡萄糖或果糖對腎細胞的影響 19 第一節 研究動機與目的 19 第二節 實驗設計、分組與材料與方法 20 一、實驗設計與分組 20 二、材料與方法 20 （一） HK-2細胞培養 20 （二） 細胞存活率測定 (MTT) 21 （三） HK-2細胞的IL-6、MCP-1與TGF-β1分泌量測定 23 （四） glucose或fructose對HK-2細胞的kim-1、 p53與caspase-3基因表現量 26 （五） 即時聚合酶連鎖反應 (Real-time PCR) 28 （六） 統計方法 29 第三節 結果 30 一、不同濃度葡萄糖或果糖對HK-2細胞存活率與細胞激素分泌的影響 30 （一）葡萄糖或果糖對HK-2細胞存活率的影響 30 （二）不同葡萄糖濃度對HK-2細胞株分泌細胞激素的影響 31 （三）不同果糖濃度對HK-2細胞株分泌細胞激素的影響 32 二、葡萄糖或果糖與LPS共處理對HK-2細胞株分泌細胞激素的影響 34 （一）低濃度葡萄糖或果糖與10-100 ng/mL LPS 34 （二）LPS濃度為500 ng/mL 35 （三）LPS濃度為1 μg/mL 36 三、葡萄糖或果糖與瘦素共處理對HK-2細胞株分泌細胞激素的影響 37 四、葡萄糖或果糖對HK-2細胞的基因表現量影響 38 第三章 探討高糖環境下葉酸營養狀況對腎細胞的影響 39 第一節 研究動機與目的 39 第二節 實驗設計、分組與材料與方法 40 一、實驗設計與分組 40 二、材料與方法 40 （一） HK-2細胞培養於缺葉酸或補充葉酸培養液 40 （二） 細胞內葉酸含量測定 41 （三） HK-2細胞的IL-6、MCP-1與TGF-β1分泌量測定 42 （四） 葉酸與高糖對HK-2細胞的kim-1、 p53與caspase-3基因表現量 43 （五） 統計方法 44 第三節 結果 45 一、HK-2細胞內葉酸含量 45 二、葉酸營養對HK-2細胞分泌細胞激素的影響 46 三、葉酸營養對高糖培養下HK-2細胞分泌細胞激素的影響 47 四、葉酸對高糖下LPS刺激HK-2細胞分泌細胞激素的影響 49 五、葉酸與葡萄糖或果糖對HK-2細胞的基因表現量影響 51 第四章GABA對腎細胞癌化的調控機制探討 52 第一節 研究動機與目的 52 第二節 實驗設計、分組與材料與方法 53 一、實驗設計與分組 53 二、材料與方法 53 （一） HK-2細胞培養 53 （二）MES-13細胞培養 53 （三） VHL siRNA轉染 54 （四） siRNA對HK-2細胞的VHL基因表現量 55 （五） 西方墨點法 (western blot) 55 （六） 氯化鈷誘導缺氧實驗 58 （七） 統計方法 59 第三節 結果 60 一、以VHL siRNA轉染HK-2細胞抑制VHL基因表現量 60 二、以VHL siRNA轉染HK-2細胞抑制VHL增加HIF-1α蛋白質表現量 61 三、以氯化鈷誘導缺氧HK-2細胞探討GABA的影響 62 四、以VHL siRNA轉染MES-13細胞抑制VHL基因表現量 63 五、以VHL siRNA轉染MES-13細胞抑制VHL增加HIF-1α蛋白質表現量 64 第五章 討論與結論 65 第一節 討論 65 一、VHL siRNA對不同細胞株的基因抑制效果 65 二、添加葡萄糖或果糖對HK-2細胞分泌細胞激素時程的影響 66 三、HK-2細胞數曲線 66 四、高糖對HK-2細胞的滲透壓 67 五、比較葡萄糖與果糖對HK-2細胞的影響 67 六、葉酸對HK-2細胞分泌IL-6的影響 68 第二節 結論 70 附錄圖 71 參考文獻 72 | |
| dc.language.iso | zh-TW | |
| dc.subject | 葉酸 | zh_TW |
| dc.subject | 糖尿病腎病變 | zh_TW |
| dc.subject | 高葡萄糖 | zh_TW |
| dc.subject | 高果糖 | zh_TW |
| dc.subject | 促發炎 | zh_TW |
| dc.subject | 纖維化 | zh_TW |
| dc.subject | fibrosis | en |
| dc.subject | folate | en |
| dc.subject | diabetic kidney disease | en |
| dc.subject | high glucose | en |
| dc.subject | high fructose | en |
| dc.subject | pro-inflammatory | en |
| dc.title | 以HK-2腎小管細胞株探討葉酸與高葡萄糖或果糖對腎的影響 | zh_TW |
| dc.title | Effects of folate and high glucose or fructose on kidney using HK-2 renal tubular cell culture | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 110-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 江孟燦(Meng-Tsan Chiang),許瑞芬(Rwei-Fen Syu),謝佳倩(Chia-Chien Hsieh),洪永瀚(Yong-Han Hong) | |
| dc.subject.keyword | 葉酸,糖尿病腎病變,高葡萄糖,高果糖,促發炎,纖維化, | zh_TW |
| dc.subject.keyword | folate,diabetic kidney disease,high glucose,high fructose,pro-inflammatory,fibrosis, | en |
| dc.relation.page | 86 | |
| dc.identifier.doi | 10.6342/NTU202202509 | |
| dc.rights.note | 同意授權(限校園內公開) | |
| dc.date.accepted | 2022-08-23 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 生化科技學系 | zh_TW |
| dc.date.embargo-lift | 2022-08-26 | - |
| 顯示於系所單位： | 生化科技學系 | |
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