Paeonol Attenuates UVB-Induced Premature Senescence in Human Dermal Fibroblasts to Promote Skin Longevity
- 1Department of Genetics & Biotechnology, Graduate School of biotechnology, College of Life Sciences, Kyung Hee University, Yongin 17104, Republic of Korea
- 2Research and Innovation Center, LABIO Co., Ltd., Seoul 08501, Republic of Korea
- 3Cosmecca Korea Co., Ltd., Seongnam 13488, Republic of Korea
Abstract
Skin photoaging is largely driven by ultraviolet (UV) irradiation, which contributes to chronic inflammation and extracellular matrix (ECM) degradation. This study investigated the protective effects of paeonol against UVB-induced cellular senescence in human dermal fibroblasts (HDFn). Repeated UVB irradiation was used to induce premature senescence. Paeonol treatment reduced the senescence-associated β-galactosidase (SA-β-gal) positive cells and intracellular reactive oxygen species (ROS) accumulation. Paeonol also reduced the expression of senescence-associated cell cycle regulators, including p21 and p16 at the mRNA level and the protein level. In addition, paeonol suppressed matrix metalloproteinase-1 (MMP-1) production but did not significantly restore type I procollagen secretion. Paeonol also attenuated the expression and secretion of the senescence-associated secretory phenotype (SASP) factors inter-leukin-6 (IL-6) and interleukin-8 (IL-8). These effects were accompanied by reduced phosphorylation of JNK and c-Jun. Furthermore, activation of JNK signaling with anisomycin partially reversed the paeonol-mediated suppression of MMP-1 mRNA expression, supporting the involvement of JNK signaling in the regulation of MMP-1. Collectively, these findings suggest that paeonol attenuates multiple features of UVB-induced cellular senescence in HDFn cells, with JNK signaling potentially contributing to its inhibitory effect on MMP-1 expression. Further studies are needed to clarify the mechanisms underlying these effects and establish their physiological relevance in UVA-based and in vivo models.
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BibTeX
@article{lee2026paeonol,
title = {{Paeonol Attenuates UVB-Induced Premature Senescence in Human Dermal Fibroblasts to Promote Skin Longevity}},
author = {Kyuri Lee and Jeung hi Han and Hairu Zhao and Young Eun Kim and Yang Gyu Choi and Hosam Ki and Jaehong Kim and Young Jin Choi and Hye Yoon Park and Areum Jang and Min Hyuk Park and Hang Eui Cho and Jae Sung Hwang},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27209352},
url = {https://www.mdpi.com/1422-0067/27/20/9352},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Paeonol Attenuates UVB-Induced Premature Senescence in Human Dermal Fibroblasts to Promote Skin Longevity
AU - Kyuri Lee
AU - Jeung hi Han
AU - Hairu Zhao
AU - Young Eun Kim
AU - Yang Gyu Choi
AU - Hosam Ki
AU - Jaehong Kim
AU - Young Jin Choi
AU - Hye Yoon Park
AU - Areum Jang
AU - Min Hyuk Park
AU - Hang Eui Cho
AU - Jae Sung Hwang
PY - 2026
DA - 2026/10/01
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27209352
UR - https://www.mdpi.com/1422-0067/27/20/9352
AB - Skin photoaging is largely driven by ultraviolet (UV) irradiation, which contributes to chronic inflammation and extracellular matrix (ECM) degradation. This study investigated the protective effects of paeonol against UVB-induced cellular senescence in human dermal fibroblasts (HDFn). Repeated UVB irradiation was used to induce premature senescence. Paeonol treatment reduced the senescence-associated β-galactosidase (SA-β-gal) positive cells and intracellular reactive oxygen species (ROS) accumulation. Paeonol also reduced the expression of senescence-associated cell cycle regulators, including p21 and p16 at the mRNA level and the protein level. In addition, paeonol suppressed matrix metalloproteinase-1 (MMP-1) production but did not significantly restore type I procollagen secretion. Paeonol also attenuated the expression and secretion of the senescence-associated secretory phenotype (SASP) factors inter-leukin-6 (IL-6) and interleukin-8 (IL-8). These effects were accompanied by reduced phosphorylation of JNK and c-Jun. Furthermore, activation of JNK signaling with anisomycin partially reversed the paeonol-mediated suppression of MMP-1 mRNA expression, supporting the involvement of JNK signaling in the regulation of MMP-1. Collectively, these findings suggest that paeonol attenuates multiple features of UVB-induced cellular senescence in HDFn cells, with JNK signaling potentially contributing to its inhibitory effect on MMP-1 expression. Further studies are needed to clarify the mechanisms underlying these effects and establish their physiological relevance in UVA-based and in vivo models.
SN - 1422-0067
ER -