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研究生: 沈虹均
Shen, Hung-Jiun
論文名稱: 松子油酸與其加長產物對於巴豆醇-12-十四烷酸酯-13-乙酸酯誘導皮膚炎的影響
Effects of pinolenic acid and its elongation product on 12-O-tetradecanoylphorbol-13-acetate-induced skin inflammation
指導教授: 蔡帛蓉
Tsai, Po-Jung
莊路德
Chuang, Lu-Te
學位類別: 碩士
Master
系所名稱: 人類發展與家庭學系
Department of Human Development and Family Studies
論文出版年: 2016
畢業學年度: 104
語文別: 中文
論文頁數: 93
中文關鍵詞: 巴豆醇-12-十四烷酸酯-13-乙酸酯脂肪酸抗發炎
英文關鍵詞: 12-O-tetradecanoylphorbol-13-acetate, fatty acids, anti-inflammatory
DOI URL: https://doi.org/10.6345/NTNU202203961
論文種類: 學術論文
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  • 皮膚炎主要為接觸性皮膚炎,由過敏源和刺激物引起。其中,刺激物引起的皮膚病佔接觸性皮膚炎病例的百分之八十。本研究利用巴豆醇-12-十四烷酸酯-13-乙酸酯(12-O-tetradecanoylphorbol-13-acetate; TPA) 誘導小鼠耳朵腫脹以及背部皮膚發炎,而使皮膚產生紅、腫的發炎反應。Pinolenic acid (PNA; 5,9,12–18:3)以及其代謝產物7-Eicosatrienoic acid (7-ETrA; 7,11,14–20:3),在細胞實驗中的抗發炎功效是本研究的基礎。我們以注射方式給予小鼠耳朵PNA與Δ7-ETrA,在不影響小鼠本身脂肪酸組成的情形下,具有顯著抑制耳朵紅腫的效果。PNA組耳朵厚度比TPA-alone組降低百分之十六,Δ7-ETrA組耳朵厚度則降低了百分之二十九ㄤ; PNA組耳朵重量比TPA-alone組降低了百分之十五,Δ7-ETrA組則降低了百分之二十二(p<0.05)‧除此之外,環氧合酶-2 (cyclooxygenase-2; COX-2)之蛋白質表現量亦受抑制,且白血球、嗜中性球及巨噬細胞也因PNA與Δ7-ETrA而顯著降低至少百分之六十七。另外我們將TPA塗抹於背部皮膚,發現PNA與Δ7-ETrA可以抑制介白素-6(interleukin-6; IL-6)、介白素-1β(interleukin-1β; IL-1β)、腫瘤壞死因子-α(tumor necrosis factor- α; TNF-α)以及前列腺素E2 (prostaglandin E2; PGE2)的生成,以及抑制促分裂原活化蛋白激酶(Mitogen-activated protein kinase; MAPK)路徑之JNK及P38磷酸化,但ERK 磷酸化無抑制效果。本研究結果顯示,PNA與Δ7-ETrA具有抑制急性皮膚發炎之功效,為預防發炎疾病開一扇窗。

    Contact dermatitis is a kind of skin inflammatory disease which is mainly caused by the allergens and irritants. Among them, irritants cause contact dermatitis is eighty percent of cases. In this study, 12-O-tetradecanoylphorbol-13-acetate (TPA) induced mouse ear edema and inflammation of the ear and dorsal skin, causing the skin red and swollen. Pinolenic acid (PNA; Δ5, 9, 12-18: 3) and its metabolites Δ7-Eicosatrienoic acid (Δ7-ETrA; Δ7, 11, 14-20: 3) in the anti-inflammatory of cell experiments was the basis of this study. We administered the mice ears PNA and Δ7-ETrA by injection, and they can inhibit ears edema significantly without changing the fatty acid composition in mice ears. Ear thickness of PNA-treated group were lower than the TPA-alone group about sixteen percent. Compared with TPA-alone group, ear thickness of Δ7-ETrA group was reduced 29 percent; ear weight of PNA-treated group was less than TPA-alone group 15 percent, and Δ7-ETrA group was reduced 22 percent (p<0.05). In addition, PNA and Δ7-ETrA also inhibit cyclooxygenase-2 (COX-2) expression, and the white blood cells, neutrophils and macrophages also reduced significantly because of PNA and Δ7-ETrA, reducing at least sixty-seven percent. In the other hand, we applied TPA on the dorsal skin, and found that PNA and Δ7-ETrA can inhibit generation of interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and prostaglandin E2 (PGE2), and inhibit mitogen-activated protein kinase (MAPK) pathway, for example, JNK and P.38 phosphorylation but not ERK phosphorylation. The results of this study showed that PNA and Δ7-ETrA inhibit the acute inflammation of the skin, and they can be the prevention of inflammatory in the future.

    中文摘要 ……………………………………………………………………………2 英文摘要………………………………………………………………………………3 目錄……………………………………………………………………………………4 第一章、緒論………………………………………………………………………...6 第一節、研究動機 …………………………………………………………….....….6 第二節、研究目的 ………………………………………………………………….7 第二章、文獻探討 ...................................................................................................8 一、皮膚構造……………………………………………………………………….8 二、皮膚炎………………………………………………………………………......9 三、巴豆醇-12-十四烷酸酯-13-乙酸酯 (TPA)誘導皮膚發炎模式…………...…..12 四、PNA及Δ7-ETrA………………………………………………………………15 五、實驗假說與設計……………………………………………………………….17 第三章、材料與方法………………………………………………………………..18 第一節、研究材料…………………………………………………………………18 一、藥品與試劑……………………………………………………………………18 二、儀器設備………………………………………………………………………25 第二節、模式建立…………………………………………………………..……..26 一、皮下注射誘導發炎模式………………………………………………………26 二、樣品製備……………………………………………………………...............27 第三節、實驗方法………………………………………………………………..28 第四章、結果 ……………………………………………………………………38 第一節、模式建立-皮下注射模式………………………………………………38 第二節、正式實驗…………………………………………………………………51 第五章、討論與結論………………………………………………………………68 第一節、討論………………………………………………………………………68 第二節、綜論與結論………………………………………………………………76 第六章 參考文獻…………………………………………………………………78

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