| 摘要: | 紫外線的照射為外因性刺激中最重要的原因之一，當皮膚暴露於太陽光，受其紫外線之影響會產生 ROS 及活化一連串訊息路徑導致發炎及光老化。近年來有許多具有活性的天然物被開發作為光保護劑。本研究選用黃酮類的 fisetin、formononetin 及 triterpene 類的 lupeol，探討其對於照射 UVB 所造成的皮膚傷害之保護。結果顯示，fisetin 於濃度 5-25 μM 時可以抑制人類纖維母細胞經 UVB 照射後所誘導之 COX-2、iNOS 及 MMP-1, -3, -9 表現量。在上游路徑探討中，可調控 MAP kinase 中的 ERK、JNK 及 p38 磷酸化，並且抑制 IκB 的磷酸化及其降解、減少進入細胞核中 NF-κB/p65 量，亦可抑制 PI3K/AKT/CREB 路徑中 p-CREB Ser 133之蛋白表現。具有開發作為光保護的潛力。lupeol 於 5-25 μM 濃度可有效地抑制因 UVB 照射誘導之 MMP-9 的表現量；formononetin 於 5-25 μM 時亦可以抑制 UVB照射所誘導的 COX-2、iNOS、MMP-1, -3, -9 及磷酸化 ERK 等蛋白質表現。由上述結果顯示，fisetin, lupeol 及 fomononetin 具有開發作為皮膚光保護劑的潛力。
Ultraviolet (UV) radiation is one of the most important extrinsic factor contributing to skin photo-damage. After UV irradiation, a series of signal transduction in skin will be activated, and leads to inflammatory response and photoaged skin. In recent years, a wide variety of natural products have been reported to possess substantial skin photoprotective effects. In this study, flavonoids, fisetin, and formononetin and triterpene, lupeol, were investigated for photoprotective effect. The results showed that fisetin at 5-25 μM could inhibit COX-2, iNOS and MMP-1, -3, -9 expression induced by UVB irradiation in human fibroblasts. In the effect of upper stream signal transduction, we found that fisetin could reduce the expression of UV-induced ERK, JNK and p38 phosphorylation in MAP kinase pahway. In addition, fisetin could reduce IκB degradation and the amount of NF-κB/p65 in cytoplasm, further more, it could suppress the expression of p-CREB Ser-133 in PI3K/AKT/CREB pathway. Lupeol could reduce the UVB-induced expression of MMP-9. Formononetin could inhibit UVB-induced COX-2, iNOS, MMP-1, -3, -9 and the phophorylation ERK expression. The mentioned effects and manchanisms suggested that fisetin, lupeol and formononetin could be potential use for development of photoprotective agents. |
