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| ???org.dspace.app.webui.jsptag.ItemTag.dcfield??? | Value | Language |
|---|---|---|
| dc.contributor.advisor | 龔秀妮 | zh_TW |
| dc.contributor.advisor | Hsiu-Ni Kung | en |
| dc.contributor.author | 王品竣 | zh_TW |
| dc.contributor.author | Pin-Jun Wang | en |
| dc.date.accessioned | 2023-10-03T17:47:11Z | - |
| dc.date.available | 2023-11-10 | - |
| dc.date.copyright | 2023-10-03 | - |
| dc.date.issued | 2023 | - |
| dc.date.submitted | 2023-08-08 | - |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/90824 | - |
| dc.description.abstract | 近年來加工食品和飲料中添加大量果糖，加劇代謝症候群的患病率，進而導致慢性腎病等器官疾病。然而，部分治療藥物存在副作用，尋找新的治療方法是必須且必要的。本研究主要探討具有抗發炎特性且傳統上被用作中草藥的山苦瓜株相關製品是否對於高果糖飲食誘導的腎臟疾病具有保護作用，利用山苦瓜葉中富含三萜類化合物區分物triterpenoid-enrichment extracts (TEE)的萃取物，探索其潛在的治療機制。
動物實驗方面，每天給予小鼠30%果糖水與TEE (150 mg/kg)，持續14週，與單純給予30%果糖水的組別比較，腎功能的多項指標，包括血壓、血清肌酸酐和尿白蛋白均得到改善。藉由組織學觀察，TEE能夠改善高果糖飲食誘導之小鼠腎絲球、近曲小管和腎小管間質區域的損傷。此外，果糖透過增加NADPH oxidase 1 (NOX1)造成腎臟的氧化壓力上升，TEE則促進NAD(P)H quinone dehydrogenase 1 (NQO1)與穀胱甘肽(Glutathione, GSH)的表現以抗衡增加的氧化壓力。除了抵抗氧化壓力之外，給予TEE能緩解由果糖引起之細胞激素前驅分子nuclear factor-kappa B (NF-κB)的活化，進而抑制細胞激素interlukin-1beta (IL-1β)、interlukin-18 (IL-18)、tumor necrosis factor-alpha (TNF-α)的表達。當氧化壓力被TEE緩解時，腎臟的發炎反應也隨之下降。隨後透過觀察肌纖維母細胞(Myofibroblast)標記:波形蛋白(Vimentin)、α-smooth muscle actin (α-SMA)與組織纖維染色(Trichrome stain)，可以發現TEE改善了由果糖所引起之小鼠腎臟纖維化。 藉由體外試驗觀察，發現近端腎小管上皮細胞HK-2受果糖和TEE的影響與小鼠實驗相似，TEE透過降低NOX1、提升NQO1以及促進穀胱甘肽(GSH)消耗來改善氧化壓力，當受果糖引起之氧化壓力被抑制後，下游發炎反應也隨之停擺。除此之外，透過HK-2進一步探討發炎反應相關之程序性細胞死亡機制:細胞焦亡(Pyroptosis)，其特性包含caspase-1活化、細胞膜產生孔洞、發炎細胞激素大量製造與釋放，果糖能夠誘發細胞焦亡與發炎反應，而給予TEE則能夠改善。此外，過去研究已證實三萜類化合物擁有促進粒線體活性的功效，為探討TEE是否擁有相同效果，首先觀察粒線體生合成與脂肪酸代謝相關分子: AMP activated protein kinase (AMPK)訊息路徑的調控，發現TEE能夠活化AMPK並開啟下游路徑，後續使用MitoView 633與MitoView Green觀察細胞粒線體功能與數量變化，果糖刺激會降低HK-2粒線體的活性與數量，而TEE的加入則能夠阻止果糖引起之傷害，大幅增加粒線體數量與功能而達到保護功效。當果糖引起之壓力被TEE消除後，HK-2轉換為肌纖維母細胞的比例減少亦與體內試驗相呼應，暗示著管道間質區域纖維化有所緩解。另一方面，系膜細胞SV40 MES13作為腎絲球血管內皮間質區域的纖維生產者，在病理形態下會增生與促進纖維製造，當腎絲球內堆積大量纖維會造成腎絲球硬化(Glomerulosclerosis)並減少過濾功能，果糖刺激後，MES13有明顯增生、纖維化以及發炎的狀況，不過這些負面的影響都在TEE加入後有所緩解。總結，在生物體方面，TEE可以保護果糖誘導之腎臟形態與功能損傷，細胞層面則能緩解果糖在近端腎小管上皮細胞以及腎絲球系膜細胞造成之傷害，故TEE在果糖引起之腎臟疾病擁有作為治療藥物的潛力。 | zh_TW |
| dc.description.abstract | In recent years, fructose enriched manufactured foods and beverages had exacerbated the incidence of metabolic syndrome, leading to chronic kidney disease and other organ diseases. However, current treatments either are not efficient or have side effects, finding new treatments is necessary. This study aims to investigate the effects of a special leaf extract [triterpenoid-enrichment extracts (TEE)] of Momordica charantia L. var. abbreviate Seringe, which is known for the anti-inflammatory properties and traditionally used as a herbal medicine, on high fructose-induced kidney disease and explore the potential therapeutic mechanisms.
In the in vivo experiments, 30% fructose water and TEE 150 mg/kg were given to mice daily for 14 weeks. Compared to the 30% fructose group, several kidney function indicators, including blood pressure, serum creatinine, and urine albumin, were improved in Fructose+TEE group. Histological observation showed that TEE ameliorated the fructose-induced damages on mouse renal glomeruli, proximal convoluted tubules, and renal tubulointerstitial area. Fructose increased kidney oxidative stress by upregulating NADPH oxidase 1 (NOX1), and TEE promoted the expression of NAD(P)H quinone dehydrogenase 1 (NQO1) and glutathione (GSH) to counteract excessive oxidative stress. TEE also alleviated the activation of the pro-inflammatory molecule nuclear factor-kappa B (NF-κB) induced by fructose, thereby inhibiting the expression of cytokines such as interlukin-1beta (IL-1β), interlukin-18 (IL-18), and tumor necrosis factor-alpha (TNF-α). In addition, TEE inhibited the fructose-induced the myofibroblast markers, vimentin and α-smooth muscle actin (α-SMA), and renal fibrosis. In the in vitro experiments, the effects of TEE on fructose treated proximal tubular epithelial cells HK-2 were similar to those in the in vivo experiments. TEE decreased fructose-induced oxidative stress by reducing NOX1, enhancing NQO1, and promoting glutathione (GSH) consumption. When oxidative stress induced by fructose is suppressed, the downstream inflammatory response also decreased by TEE. Additionally, fructose can induce pyroptosis, which is characterized by the activation of caspase-1, hole formation in the cell membrane, and massive manufacture and release of inflammatory cytokines in HK-2, and TEE can significantly inhibit both phenomena. Fructose also decreased the activity and quantity of mitochondria in HK-2, while the addition of TEE can prevent fructose's negative regulation on mitochondria to achieve the protective effect by activacting AMP activated protein kinase (AMPK). The transformation of HK-2 to myofibroblasts was increased by fructose and decreased by TEE administration, which suggesting an alleviation in interstitial fibrosis. On the other hand, Fructose stimulation causes notable proliferation, fibrosis, and inflammation in mesangial cells SV40 MES13, are fiber producers in the glomerular vascular endothelium interstitial region, but these negative effects were alleviated with the addition of TEE. In conclusion, on the mouse level, TEE can protect the fructose-induced morphological and functional renal damages . On the cellular level, TEE can alleviate the damaged caused by fructose in proximal tubular epithelial cells and glomerular mesangial cells. Therefore, TEE had the potential serving as a therapeutic agent for fructose-induced kidney diseases. | en |
| dc.description.provenance | Submitted by admin ntu (admin@lib.ntu.edu.tw) on 2023-10-03T17:47:11Z No. of bitstreams: 0 | en |
| dc.description.provenance | Made available in DSpace on 2023-10-03T17:47:11Z (GMT). No. of bitstreams: 0 | en |
| dc.description.tableofcontents | 第一章 緒論 1
第一節 引言 1 第二節 腎臟 2 一、基本結構 2 二、組織學與其生理功能 3 第三節 高果糖飲食與腎損傷之關係 6 一、簡介 6 二、吸收、代謝機制 6 三、過量果糖引起之損傷途徑 8 四、氧化壓力與抗氧化系統 11 五、發炎反應與細胞焦亡(Pyroptosis) 14 六、上皮細胞間質轉化(Epithelial-mesenchymal transition, EMT)與纖維化 18 第四節 山苦瓜葉萃取物的生理活性 19 第五節 研究動機 21 一、實驗假說 21 二、實驗架構 21 第二章 材料與方法 22 第一節 材料與儀器 22 一、富含三萜類萃取物(Triterpenoid-enriched extract, TEE) 22 二、動物實驗 22 三、細胞實驗 22 四、實驗藥品 23 五、試劑儀器 24 第二節 山苦瓜葉萃取物 25 一、烘乾磨粉 25 二、山苦瓜葉出萃取物BMLE (Bitter melon leaves extract) 26 三、山苦瓜葉萃取物TEE (Triterpenoid-enriched extract) 26 第三節 動物實驗 27 一、實驗動物 27 二、實驗設計 27 第四節 細胞實驗 30 一、細胞培養 30 二、實驗設計 30 第五節 實驗技術 33 一、小鼠尾靜脈血壓測量儀Blood pressure 33 二、血清及尿液生化分析 33 三、石蠟包埋與切片 35 四、蘇木素-伊紅染色(Hematoxylin-Eosin stain) 35 五、碘酸雪夫氏染色(Periodic acid-Schiff stain, PAS) 36 六、馬森三色染色法(Masson’s Trichome stain) 36 七、免疫組織螢光染色(Immunofluorescence, IF) 37 八、免疫細胞螢光染色(Immunofluorescence, IF) 38 九、細胞計數(Cell counting) 38 十、結晶紫(Crystal violet) 39 十一、細胞存活率測試(MTT assay) 39 十二、細胞存活率測試(CCK-8 assay) 39 十三、流式細胞儀(Flow cytometry) 39 十四、細胞螢光染色 39 十五、西方墨點法(Western blot) 40 十六、穀胱甘肽(Glutathione, GSH)測試 44 十七、丙二醛(Malondialdehyde, MDA)測試 44 十八、即時聚合酶連鎖反應(Real-time polymerase chain reaction, qPCR) 44 十九、海馬生物能量測定 47 第六節 統計分析 47 第三章 結果 48 第一節 TEE改善由果糖引起之小鼠體重及腎重增加 48 第二節 TEE緩解高果糖飲食對小鼠生理狀態之影響 48 第三節 TEE改善由高果糖飲食引起之腎臟型態損傷 49 第四節 TEE降低由高果糖飲食引起之小鼠腎臟發炎反應 50 第五節 TEE改善由高果糖飲食所誘導之小鼠腎臟氧化壓力狀態 50 第六節 TEE改善由高果糖飲食引起之腎臟纖維化 51 第七節 果糖引起HK-2細胞發炎 52 第八節 果糖促使HK-2細胞氧化壓力增加 53 第九節 果糖增加HK-2細胞內NF-κB的轉位作用 53 第十節 果糖透過增加氧化壓力引起HK-2細胞發炎反應 54 第十一節 TEE改善由果糖引起之HK-2細胞發炎反應 54 第十二節 TEE回復由果糖引起之HK-2細胞焦亡(Pyroptosis) 55 第十三節 TEE降低果糖引起之HK-2氧化壓力 56 第十四節 TEE改善果糖引起之HK-2粒線體功能與數量損傷 57 第十五節 TEE改善果糖引起之HK-2上皮細胞間質轉化(Epithelial-mesenchymal transition, EMT) 59 第十六節 果糖增加SV40 MES13細胞數量並引起纖維化 59 第十七節 果糖促使SV40 MES13細胞產生發炎反應 60 第十八節 TEE改善由果糖引起之SV40 MES13細胞纖維化與發炎反應 60 第四章 討論 62 第一節 簡述 62 第二節 果糖造成的HK-2氧化壓力上升是否起源於尿酸 63 第三節 TEE透過活化粒線體抵銷果糖引起HK-2之瓦博格效應 63 第四節 果糖不會透過引起SV40 MES13氧化壓力造成纖維化 64 第五節 探討果糖引起SV40 MES13發炎反應之途徑 64 第六節 比較GSH在組織與HK-2內的變化量 65 第七節 過量TEE可能降低HK-2粒線體功能 66 第五章 結論 68 第六章 附圖 70 第七章 參考文獻 120 第八章 附錄 131 | - |
| dc.language.iso | zh_TW | - |
| dc.subject | 腎損傷 | zh_TW |
| dc.subject | 近端腎小管上皮 | zh_TW |
| dc.subject | 腎絲球系膜細胞 | zh_TW |
| dc.subject | 氧化壓力 | zh_TW |
| dc.subject | 發炎 | zh_TW |
| dc.subject | 纖維化 | zh_TW |
| dc.subject | 天然萃取物 | zh_TW |
| dc.subject | 高果糖飲食 | zh_TW |
| dc.subject | TEE | en |
| dc.subject | High-fructose Diet | en |
| dc.subject | Renal Injury | en |
| dc.subject | Proximal Tubular Epithelium | en |
| dc.subject | Mesangial Cells of the Glomerulus | en |
| dc.subject | Oxidative Stress | en |
| dc.subject | Inflammation | en |
| dc.subject | Fibrosis | en |
| dc.subject | Natural Extracts | en |
| dc.title | 富含三萜類山苦瓜葉萃取物對高果糖飲食誘導腎臟損傷之保護作用 | zh_TW |
| dc.title | The protective effect of wild bitter melon leaf extract enriched triterpenoids against high-fructose diet induced kidney injuries | en |
| dc.type | Thesis | - |
| dc.date.schoolyear | 111-2 | - |
| dc.description.degree | 碩士 | - |
| dc.contributor.oralexamcommittee | 林甫容;劉興華;蔡帛蓉;周逸鵬 | zh_TW |
| dc.contributor.oralexamcommittee | Fu-Jung Lin;Shing-Hwa Liu;Po-Jung Tsai;Yat-Pang Chau | en |
| dc.subject.keyword | 高果糖飲食,腎損傷,近端腎小管上皮,腎絲球系膜細胞,氧化壓力,發炎,纖維化,天然萃取物, | zh_TW |
| dc.subject.keyword | High-fructose Diet,Renal Injury,Proximal Tubular Epithelium,Mesangial Cells of the Glomerulus,Oxidative Stress,Inflammation,Fibrosis,Natural Extracts,TEE, | en |
| dc.relation.page | 136 | - |
| dc.identifier.doi | 10.6342/NTU202303666 | - |
| dc.rights.note | 同意授權(全球公開) | - |
| dc.date.accepted | 2023-08-09 | - |
| dc.contributor.author-college | 醫學院 | - |
| dc.contributor.author-dept | 解剖學暨細胞生物學研究所 | - |
| dc.date.embargo-lift | 2028-08-08 | - |
| Appears in Collections: | 解剖學暨細胞生物學科所 | |
Files in This Item:
| File | Size | Format | |
|---|---|---|---|
| ntu-111-2.pdf Until 2028-08-08 | 6.83 MB | Adobe PDF |
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