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.

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