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miR-34c, 高脂肪飲食和神經退化性疾病的相關研究

為了解決VITA 300 PTT的問題，作者高毓佳 這樣論述：

神經退化性疾病縱然在部分病患有遺傳傾向，環境因素亦可藉由表觀遺傳(epigenetic)之調控影響疾病的危險性和影響病程進展，此一論文旨在研究轉錄後及轉譯後調控方式一為微核糖核酸，另一為飲食對前兩大神經退化性疾病阿茲海默症和巴金森氏症的影響。微核糖核酸(miRNAs)逐漸被視為神經退化性疾病的關鍵調控因子。在第一個研究中我們假設表現於海馬迴的微核糖核酸-34c於老鼠會引發如同人類阿茲海默症之記憶障礙，我們證實微核糖核酸-34c過量表現於海馬迴神經元會對神經樹突長度和神經樹突棘密度造成負向影響，將微核糖核酸-34c感染載入之海馬迴神經元相較未被感染載入之神經元平均神經樹突較短且有較少之絲狀偽足

(filopodia)。神經樹突和突觸為神經傳導乃至記憶形成和儲存的基本結構，神經樹突的破壞足以引發阿茲海默症。飲食對健康至關重要且為簡易可調整的因子，流行病學及動物實驗顯示代謝性疾病包含肥胖和神經退化性疾病的相關性。第二個實驗旨在研究飲食引發之肥胖對巴金森氏症之影響，著重於多巴胺路徑和腦部過氧化體增生活化受體。高脂飲食造成老鼠腦部黑質多巴胺神經元數量降低，高脂飲食亦促發神經發炎造成黑質和紋狀體星形膠質細胞增生，腦部黑質之神經樹突棘減少顯示長期高脂飲食改變多巴胺神經之神經可塑性。高脂飲食餵食之老鼠其腦部黑質和腹側被蓋區之所有過氧化體增生活化受體子型(α, β/δ, γ)之數量皆比一般飲食之對照

組減少，其中又以α子型之減少最為顯著。

以電腦模擬、體外、體內與奈米吸附篩選及印證天然化合物

為了解決VITA 300 PTT的問題，作者THIYAGARAJAN VARDHARAKAN 這樣論述：

Focal adhesion kinase (FAK) is a nonreceptor protein tyrosine has been overexpressed in many types of tumors and plays an important role in number of cell signaling pathways including cell migration, proliferation, viability, and cell survival. This study was aimed to identify the novel and specifi

c inhibitors from natural compounds via molecular docking of FAK (Y397) and investigate the underlying mechanism of action. The 3D structure of the FAK (PDB ID: 2AL6) was used for docking 107 Natural compounds. Based on their high affinity and energy interaction, top two compounds Antroquinonol from

Antrodia camphorata and 16-hydroxy-cleroda-3,13-dien-16,15-olide (HCD) from Polyalthia longifolia were selected and further validated with C6 Glioma and N18 Neuroblastoma cell lines. Protein (2AL6) - ligands interaction analysis indicated that H-bond with residues Arg 86 and Arg 125. These compoun

ds showed a potential effect on cell viability by MTT assay; in contrast cell cycle analysis showed cell arrest in subG1 and G0-G1 phase, respectively and further induction of apoptosis was confirmed by TUNEL assay. Atomic Force Microscopy data depicted that the formation of filopodia on intracellu

lar surface decreased in treated cells as compared to the control. In addition, both compounds inhibited the activity of MMP 2 and 9 using Zymography. The protein levels of FAK, pFAK, Rac1 and cdc 42 were decreased, which are the key regulators for the formation of filopodia and cell migration. Fur

ther, both the compounds regulate the expression of epithelial mesenchymal transition (EMT) proteins. HCD and antroquinonol induce the autophagy through ROS mechanism. Further, HCD conjugated with Cu-MSN showed a controlled drug release and reduced the tumor growth of glioma. Taken together, this st

udy suggests that Antroquinonol and 16-hydroxy-cleroda-3,13-dine-16,15-olide could be a potential inhibitor of FAK for anti-tumorigenesis and anti-metastasis.