Wen Su-Ying, Ng Shang-Chuan, Noriega Lloyd, Chen Tzu-Jung, Chen Chih-Jung, Lee Shin-Da, Huang Chih-Yang, Kuo Wei-Wen
Department of Dermatology, Taipei City Hospital, Zhongxing Branch, Taipei, Taiwan, ROC.
Department of Cosmetic Applications and Management, Mackay Junior College of Medicine, Nursing, and Management, Taipei, Taiwan, ROC.
Biofactors. 2025 Jan-Feb;51(1):e2152. doi: 10.1002/biof.2152.
Ultraviolet (UV) irradiation is a major factor contributing to skin photoaging, including the formation of reactive oxygen species (ROS), collagen breakdown, and overall skin damage. Insulin-like growth factor-I (IGF-1) is a polypeptide hormone that regulates dermal survival and collagen synthesis. Echinacoside (Ech), a natural phenylethanoid glycoside, is the most abundant active compound in Cistanches. However, its potential benefits for the skin and the underlying molecular mechanisms remain unclear. The objective of this research is to investigate the protective effect of Ech on human dermal fibroblast cells (HDFs) against UVB-induced skin photodamage. In this study, we demonstrated that Ech promotes IGF-1/IGF-1R/ERK-mediated collagen synthesis and IGF-1/IGF-1R/PI3K-mediated survival pathways, as well as induces IGF-1 secretion to counteract UVB-induced aging in HDFs. Furthermore, UVB-induced accumulation of SA-β-gal-positive cells, ROS, and impaired collagen synthesis were attenuated following Ech treatment. However, the protective effects of Ech were significantly diminished when IGF-1 and IGF-1R expression was silenced using small interfering RNA, indicating that Ech exerts its antiaging effects primarily by activating the IGF-1/IGF-1R signaling pathway. Our findings provide evidence of the antiaging effects of Ech on UVB-induced skin photodamage and suggest its potential development as a supplement in cosmetic dermal protective products.
紫外线（UV）照射是导致皮肤光老化的主要因素，包括活性氧（ROS）的形成、胶原蛋白分解以及整体皮肤损伤。胰岛素样生长因子-I（IGF-1）是一种调节真皮存活和胶原蛋白合成的多肽激素。松果菊苷（Ech）是一种天然苯乙醇苷，是肉苁蓉中含量最丰富的活性化合物。然而，其对皮肤的潜在益处及潜在分子机制仍不清楚。本研究的目的是探讨松果菊苷对人皮肤成纤维细胞（HDFs）抗UVB诱导的皮肤光损伤的保护作用。在本研究中，我们证明松果菊苷促进IGF-1/IGF-1R/ERK介导的胶原蛋白合成和IGF-1/IGF-1R/PI3K介导的存活途径，并诱导IGF-1分泌以对抗UVB诱导的HDFs衰老。此外，松果菊苷处理后，UVB诱导的SA-β-半乳糖苷酶阳性细胞积累、ROS生成及胶原蛋白合成受损均得到减轻。然而，当使用小干扰RNA沉默IGF-1和IGF-1R表达时，松果菊苷的保护作用显著减弱，表明松果菊苷主要通过激活IGF-1/IGF-1R信号通路发挥其抗衰老作用。我们的研究结果为松果菊苷对UVB诱导的皮肤光损伤的抗衰老作用提供了证据，并表明其作为化妆品皮肤保护产品中的一种补充剂具有潜在的开发价值。
