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咖啡莓果水萃物對小鼠腦部和肝臟之凋亡蛋白酶非依賴性細胞凋亡與自噬作用之影響

為了解決NICE XL PTT的問題，作者林雨璇 這樣論述：

隨著年齡的增加，會因為細胞累積的損傷，造成器官受損和功能障礙。阿茲海默症(Alzheimer's disease, AD)是常見的老年退化性疾病，病理特徵為患者腦部有大量類澱粉蛋白(β-amyloid, Aβ)沉積和神經纖維纏結(neurofibrillary tangles, NFTs)，使腦神經系統退化，進而造成學習記憶功能衰退。非酒精性脂肪肝(non-alcoholic fatty liver disease, NAFLD)則是一種因脂肪囤積引起肝細胞受到破壞的疾病總稱，在老年族群亦有較高的發生率。咖啡莓果(coffeeberry, CB)是咖啡樹之果實，富含多酚類物質，具有良好的抗氧

化能力。先前本實驗室已證實咖啡莓果水萃物(coffeeberry water extract, CBWE)具有降低發炎反應、提升神經滋養因子，但其對凋亡和自噬途徑的影響尚不清楚。本研究目的為探討給予SAMP8小鼠CBWE後，透過凋亡和自噬途徑對AD和NAFLD這兩個疾病的影響。實驗選用3月齡雄性SAMP8小鼠，分為控制組、補充CBWE 10.24、20.48和40.96mg/kg BW共四組，每週紀錄體重及攝食量，為期12週。動物犧牲後測量皮質、海馬迴和肝臟中之聚腺嘌呤雙磷酸核糖聚合酶 1(poly(ADP-ribose) polymerase 1, PARP 1)、促凋亡因子(apoptos

is inducing factor, AIF)、熱休克蛋白 70(heat shock proteins 70, Hsp70)、沉默調節蛋白(silence information regulator 1, Sirt 1)、哺乳動物雷帕黴素目標蛋白(mammalian target of rapamycin, mTOR)、P70S6激酶(P70 S6 kinase, P70S6K)、自噬活化因子─Beclin 1和微管相關蛋白輕鏈3-II(microtubule-associated proteins 3-II, LC3-II)，並檢測血清生化值和肝臟抗氧化指標。結果顯示，補充CBWE能減少

皮質和海馬迴之MDA含量，此外，亦可以降低PARP 1的過度活化和裂解，並提升Hsp70的表現，因而減緩了AIF所產生的細胞毒性，進而抑制細胞凋亡的現象；CBWE亦可增加Sirt 1的表現，減少了mTOR和P70S6K的磷酸化，提升了Beclin 1和LC3-II之蛋白表現，進而促進自噬作用。此外，CB在肝臟組織可降低脂質和蛋白質的氧化，抑制細胞凋亡和促進自噬作用的相關蛋白表現，進而有效改善肝功能指標。綜合以上，CBWE可降低氧化壓力和凋亡因子的表現，增加自噬因子的產生，可能藉此延緩年齡增長所造成可能的細胞損傷。

新穎性長鏈烴基醯胺衍生物WMJ-S-001之抗腫瘤機轉與介白質-6誘導淋巴管新生之作用探討

為了解決NICE XL PTT的問題，作者黃愈涵 這樣論述：

To date, cancer remains a major cause of death worldwide. Despite advances in drug discovery and the use of targeted therapies in recent years, the prognosis for many advanced cancers remains poor. Therefore, developing novel agents or therapies is an ongoing urgent need for cancer treatment. Recen

t development in drug discovery has highlighted the broad pharmacological properties of a key pharmacophore, hydroxamate, although the exact mechanisms remain unclear. We have synthesized a series of aliphatic hydroxamate derivatives, the WMJ-S compounds, and evaluated their anti-tumor activities. A

mong these WMJ-S compounds, WMJ-S-001 exhibits the most potent cytotoxicity in cancer cells. We thus selected WMJ-S-001 and investigated the mechanisms by which WMJ-S-001 induces HCT116 colorectal cancer cell death (Part I). We have demonstrated that the death of HCT116 colorectal cancer cells expos

ed to WMJ-S-001 may involve AMPK-p38MAPKp53-survivin cascade. These results support the role of WMJ-S-001 as a potential drug candidate and warrant the clinical development in the treatment of cancer. On the other hand, the dilemma of anti-cancer agent development is attributed to the complexity of

tumor progression. An understanding of the mechanisms underlying tumor progression is another major issue for cancer research. Growing evidences have shown that elevated serum IL-6 is associated with advanced stages and poor prognosis of colorectal cancer. Moreover, IL-6 has been shown to promote tu

mor lymphangiogenesis and metastasis through vascular endothelial growth factor-C (VEGF-C) induction in tumor cells. Whether IL-6 induces VEGF-C expression in lymphatic endothelial cells (LECs) and its underlying mechanisms remain unclear. In this study, we also investigate the precise mechanisms un

derlying IL-6-induced VEGF-C expression in LECs (Part II). We report a Src-FAK-mediated STAT3, C/EBPβ and p65 activation leading to VEGF-C expression and lymphangiogenesis in IL-6/sIL-6R-exposed SV-LECs. The identification of mechanisms underlying IL-6/sIL-6R-associated tumor lymphangiogenesis will

aid in future development of new selective-targeting strategies in the treatment of cancer.