Arctigenin protects against ultraviolet-A-induced damage to stemness through inhibition of the NF-κB/MAPK pathway
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Updated: Feb 15, 2026

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C UV-C Damage
Published on: February 15, 2020
See-Hyoung Park1, Jae Youl Cho2, Sae Woong Oh2
1Department of Bio and Chemical Engineering, Hongik University, 300-16 Sejong City, Republic of Korea.
Abstract:
The stemness of stem cells is negatively affected by ultraviolet A (UVA) irradiation. This study was performed to examine the effects of arctigenin on UVA-irradiation-induced damage to the stemness of human mesenchymal stem cells (hMSCs) derived from adipose tissue. The mechanisms of action of arctigenin were also investigated. A BrdU-incorporation assay demonstrated that arctigenin attenuated the UVA-induced reduction of the cellular proliferative potential. Arctigenin also increased the UVA-induced reduction in stemness of hMSCs by upregulating stemness-related genes such as SOX2, OCT4, and NANOG. In addition, the UVA-induced reduction in the mRNA expression level of hypoxia-inducible factor (HIF)-1α was significantly recovered by arctigenin. The antagonizing effect of arctigenin on UVA irradiation was mediated by reduced PGE2 production through the inhibition of MAPKs (p42/44 MAPK, p38 MAPK, and JNK) and NF-κB. Overall, these findings suggest that arctigenin can ameliorate the reduced stemness of hMSCs induced by UVA irradiation. The effects of arctigenin are mediated by PGE2-cAMP signaling-dependent upregulation of HIF-1α. Therefore, arctigenin could be used as an antagonist to attenuate the effects of UVA irradiation.
Insights
Arctigenin protects human mesenchymal stem cells from UV damage, preserving their stemness and proliferative capacity. This natural compound upregulates key stemness genes and restores hypoxia-inducible factor-1α levels, offering a potential therapeutic strategy against UV-induced cellular damage.
Area of Science:
- Stem Cell Biology
- Dermatology
- Pharmacology
Background:
- Ultraviolet A (UVA) irradiation negatively impacts stem cell stemness.
- Human mesenchymal stem cells (hMSCs) are crucial for tissue repair and regeneration.
- Protecting hMSC stemness from environmental damage is vital for therapeutic applications.
Purpose of the Study:
- To investigate the protective effects of arctigenin against UVA-induced damage to hMSC stemness.
- To elucidate the underlying mechanisms of arctigenin's action.
Main Methods:
- BrdU-incorporation assay to assess cellular proliferation.
- Quantitative analysis of stemness-related gene expression (SOX2, OCT4, NANOG).
- Measurement of hypoxia-inducible factor (HIF)-1α mRNA levels.
- Investigation of signaling pathways involving PGE2, MAPKs, and NF-κB.
Main Results:
- Arctigenin counteracted UVA-induced reduction in hMSC proliferative potential.
- Arctigenin upregulated SOX2, OCT4, and NANOG, preserving stemness.
- Arctigenin restored UVA-induced decrease in HIF-1α mRNA expression.
- The protective effect involved reduced PGE2 production via inhibition of MAPKs and NF-κB.
Conclusions:
- Arctigenin ameliorates UVA-induced stemness reduction in hMSCs.
- The mechanism involves PGE2-cAMP signaling-dependent upregulation of HIF-1α.
- Arctigenin shows potential as an antagonist against UVA irradiation effects.
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