PEPTIDES A UV 20mJ No treatment UV 20mJ +MetaTlr (40ug/ml) 1.5 ** 1.0 ** 0.5 * * MetaTlr (40ug/ml) ■ Control


■ UV ■ Meta TLR


B C SA-β-gal staining NC


51


0.0 IL-1β IL-6 LMNB1 COL1A1 HFF-1 Bar=300um


Figure 3: The senopreventive peptide alleviates intrinsic ageing and UVB-induced photoageing. (A) Image of HFF-1 after UV irradiation with/without the senopreventive peptide. (B) mRNA expression after UV irradiation with/without the senopreventive peptide. (C) SA-β-gal staining of UV irradiation of HFF-1 cells


reduced β-Hexosaminidase release in response to stimulator Substance P, suggesting its potential to inhibit mast cell degranulation and modulate mast cell-driven inflammation. In co-cultures of SH-SY5Y neuroblastoma


cells and HaCaT keratinocytes, 10 ng/mL TNF-α treatment led to an increase in neuropeptide Substance P (SP) secretion, which further induced IL-6 and IL-1β secretion. Treatment with the senopreventive peptide significantly suppressed


SP, IL-6, and IL-1β release, indicating its potential to both suppress the initiation of inflammatory responses and modulate downstream signaling.


The senopreventive peptide alleviates intrinsic ageing and UVB-induced photoageing Exposure to UVB radiation, as a significant contributor to extrinsic skin ageing, causes oxidant stress and inflammation. The senopreventive peptide treatment effectively alleviated the


morphological changes in HFF-1 cells induced by UVB irradiation. RT-qPCR analysis revealed that the senopreventive peptide decreased the expression of inflammation marker IL-6/IL-1β, and MMP1 (ECM degradation enzyme), p21 (cell cycle regulator, marker of cellular senescence), and increased the expression of Lamin B1 and Collagen I, critical markers of cellular senescence and wrinkle formation, indicating that the senopreventive peptide protects against UVB-induced senescence.


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September 2026 PERSONAL CARE MAGAZINE


Relative mRNA expression


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