Correlation of bioactive components of platelet rich plasma derived from human female adult peripheral blood and umbilical cord blood with age.

Platelet-rich plasma (PRP) has gained significant attention in the field of regenerative medicine due to its potential therapeutic applications. However, few studies have reported the components, especially anti-ageing-related components, of PRP derived from umbilical cord blood (UCB). It is essential to understand the influence of age on the composition and efficacy of PRP to optimize its clinical use. The present study compared the concentrations of bioactive components in PRP from healthy female adults and UCB-derived PRP. PRP was obtained from blood samples from females in four age groups (12 per group): neonates (UCB donors) and adults aged 18-25, 26-45, and 46-65 years, respectively. The concentrations of epidermal growth factor, basic fibroblast growth factor-2 (FGF-2), insulin-like growth factor-1, platelet-derived growth factor-AA (PDGF-AA), PDGF-AB/BB, vascular endothelial growth factor A, RANTES, TIMP-1, TIMP-2, GDF11, and clusterin and activity of superoxide dismutase, catalase, and glutathione peroxidase (GPx) in the PRP samples were determined and compared among groups. Pairwise comparisons between the groups showed statistically significant differences in the concentrations of some bioactive components of PRP, such as FGF-2, PDGF-AB/BB, and clusterin, and GPx activity. UCB-derived PRP contains various active ingredients such as VEGF-A, CAT activity, and TIMP-2. Contrary to expectations, UCB-derived PRP did not show higher concentrations of the anti-ageing protein GDF11. Because UCB is a rich source of bioactive components with low immunogenicity, its use in PRP preparation is an important research direction for future studies.

Platelet-rich plasma protects human melanocytes from oxidative stress and ameliorates melanogenesis induced by UVB irradiation.

To investigate the role of platelet-rich plasma (PRP) from different sources in alleviating oxidative stress and ameliorating melanogenesis in UVB-irradiated PIG1 cells, PIG1 cells were irradiated with 80 mJ/cm2 UVB prior to 1% PRP application and the following experiments were taken: the viability of UVB-irradiated PIG1 cells, cellular malondialdehyde (MDA) and reactive oxygen species (ROS) content, and activities of antioxidant enzymes. Western blotting was utilized to detect the expression level of proteins associated with melanin synthesis, apoptosis, and DNA lesions. We found that PRP intervention promoted cell proliferation, reduced MDA and ROS content, increased the activities of series of antioxidant enzymes, and alleviated DNA damages in UVB-damaged PIG1 cells. It is important to note that PRP treatment inhibited UVB-induced melanogenesis via the PI3K/Akt/GSK3ß signal pathway. Therefore, we suppose PRP treatment exerts a protective role through their antioxidation effect on UVB-damaged PIG1 cells and hinders melanogenesis induced by UVB irradiation.

The Anti-photoaging Effects of Pre- and Post-treatment of Platelet-rich Plasma on UVB-damaged HaCaT Keratinocytes.

Platelet-rich plasma (PRP) has seen wide clinical use owing to its regenerative and repair abilities. OBJECTIVE: To investigate the anti-photoaging effects of pre- and post-treatment of PRP on UVB-damaged HaCaT cells. METHODS: HaCaT cells were irradiated with 80 mJ/cm2 UVB, before or after PRP treatment (1000 × 107 /L), and following measurements were taken: survival rate of UVB-irradiated HaCaT cells, malondialdehyde (MDA) content and activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT). Western blot was used to determine the effect of different PRP intervention on the expression of PI3K, AKT, ERK, MMP-1, MMP-9, TIMP-1 and γ-H2AX in the UVB-irradiated HaCaT cells. RESULTS: pre- and post-PRP treatment reduced MDA content and increased the activities of GSH-Px, SOD and CAT in photoaged HaCaT cells. These changes resulted in reduced cytotoxic effects. Besides, different PRP intervention promoted cell proliferation via PI3K/AKT pathway. Furthermore, PRP application suppressed the expression of γ-H2AX. Also, PRP intervention alleviated photoaging effects by upregulating the expression level of tissue inhibitor of metalloproteinases-1 (TIMP-1) while downregulating matrix metalloproteinase (MMP) expression level in photoaged HaCaT cells. CONCLUSION: pre- and post-PRP treatment play anti-photoaging role through strengthening cellular oxidative defense capacity, mitigating MMP expression, alleviating DNA damages and promoting proliferation of UVB-irradiated HaCaT cells.