MSC-Exosomes Hypoxia (EH-MSCs) in modulating Apaf-1 and Survivin in UVB-induced skin aging
Skin aging is marked by decreased elasticity and increased wrinkle formation, often associated with altered expression of key genes such as APAF-1 and Survivin. Exposure to UVB radiation, particularly in tropical regions, accelerates collagen degradation, thereby heightening the risk of premature aging. Mesenchymal stem cell-derived hypoxic exosomes (MSCs-Exosome Hipoksia) have shown potential in suppressing APAF-1 expression and enhancing Survivin levels, although their effects on UVB-induced skin damage have not been fully explored. This study investigated the impact of MSCs-Exosome Hipoksia on APAF-1 and Survivin gene expression in UVB-exposed rat skin. Rats with reduced collagen levels due to UVB exposure were randomly assigned into four groups: normal control (KN; UVB + 0.9% sodium chloride 300 µL), positive control (KP; UVB + hyaluronic acid 200 µL), treatment group 1 (T1; UVB + MSCs-Exosome Hipoksia 200 µL), and treatment group 2 (T2; UVB + MSCs-Exosome Hipoksia 300 µL). The T2 group demonstrated the lowest APAF-1 expression (1.03 ± 0.33 pg/mL) and the highest Survivin expression (4.35 ± 0.73 pg/mL). Both treatment groups (T1 and T2) showed statistically significant reductions in APAF-1 and increases in Survivin expression compared to control groups (p < 0.05). These findings indicate that MSCs-Exosome Hipoksia, particularly at a dose of 300 µL, may effectively modulate molecular markers associated with skin aging and hold therapeutic potential in mitigating UVB-induced dermal damage.
Authors
- Agung Putra (ORCID: https://orcid.org/0000-0003-4261-9437)
- Eko Setiawan (ORCID: https://orcid.org/0000-0002-7194-2359)
- Citra Megawati Agustina
Institutions
- Sultan Agung Islamic University (ID)
Publication Details
- Journal
- Jurnal Teknologi Laboratorium
- Published
- 2025-05-21
- DOI
- https://doi.org/10.29238/teknolabjournal.v14i1.541
- Primary Topic
- Skin Protection and Aging
- Type
- article
- Field-Weighted Citation Impact
- 0.00