Echinacoside promotes collagen synthesis and survival via activation of IGF-1 signaling to alleviate UVB-induced dermal fibroblast photoaging.

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. © 2025 International Union of Biochemistry and Molecular Biology.

Citation

Su-Ying Wen, Shang-Chuan Ng, Lloyd Noriega, Tzu-Jung Chen, Chih-Jung Chen, Shin-Da Lee, Chih-Yang Huang, Wei-Wen Kuo. Echinacoside promotes collagen synthesis and survival via activation of IGF-1 signaling to alleviate UVB-induced dermal fibroblast photoaging. BioFactors (Oxford, England). 2025 Jan-Feb;51(1):e2152

Mesh Tags

Substances

PMID: 39780317

search → result