PDRN

PDRN induces cell growth in human primary dermal fibroblasts, and this effect depends on the activation of adenosine A_2a receptor^[1].
PDRN (20 mg/mL) promotes the proliferation of cultured human osteoblasts and enhances their alkaline phosphatase activity, and this effect is mediated through the activation of adenosine A_2a receptor^[1].
PDRN promotes extracellular matrix preservation and reduces its degradation in primary human chondrocytes, and exerts a synergistic effect when combined with Glucosamine (HY-B1125)^[1].
PDRN promotes the proliferation of human preadipocytes, supporting its potential application in regenerative medicine^[1].
PDRN supports the activity of DNA salvage pathways in cultured human dermal fibroblasts and promotes cell proliferation through nucleotide internalization and integration^[1].
PDRN protects human skin fibroblasts against UVB-induced DNA damage by activating p53 and enhancing DNA repair via the salvage pathway^[1].
PDRN (10-200 µg/mL; 4 days) reduces melanin content in melanocytes from Mel-Ab mice in a dose-dependent manner. After 4 days of treatment, the highest tested concentration (200 µg/mL) decreases melanin content to approximately 60% of that in the untreated control group^[2].
PDRN (50-100 µg/mL; 5 days) reduces melanin content in a human melanocyte-keratinocyte co-culture system in a dose-dependent manner. After 5 days of treatment, the melanin content in the 100 µg/mL group decreases to approximately 75% of that in the untreated control group^[2].
PDRN (10-200 µg/mL; 4 days) significantly reduces tyrosinase activity in melanocytes of Mel-Ab mice. After 4 days of treatment, the 50 µg/mL dose decreases the enzyme activity to approximately 25% of that in the untreated control group, while the 100 and 200 µg/mL doses reduce the enzyme activity to approximately 35% of that in the untreated control group^[2].
PDRN (100 µg/mL; 24-72 h) reduces the protein levels of MITF, TRP-1 and tyrosinase in melanocytes from Mel-Ab mice^[2].
PDRN (100 µg/mL; 10-360 min) transiently increases the levels of phosphorylated ERK and AKT in melanocytes of Mel-Ab mice, with the activation peak of ERK occurring at 10 min and that of AKT at 30 min; meanwhile, this substance causes a fluctuating increase in phosphorylated GSK3β levels, but exerts no effect on the levels of β-catenin, total ERK, total AKT, and total GSK3β^[2].
PDRN (800 μg/mL; 24 h) improves the viability of HaCaT human keratinocytes subjected to UVB- or H₂O₂-induced stress^[3].
PDRN (800 μg/mL; 24 h) significantly reduces apoptosis of human keratinocyte HaCaT cells induced by UVB or H₂O₂^[3].
PDRN (800 μg/mL; 12-24 h) enhances the migratory capacity of HaCaT human keratinocytes subjected to UVB- or H₂O₂-induced stress^[3].
PDRN (800 μg/mL; 24 h) attenuates UVB- or H₂O₂-induced senescence in human keratinocyte HaCaT cells^[3].
PDRN (800 μg/mL; 24 h) reduces the formation of SIRT1 stress granules, nucleophagy, and LC3-SIRT1 colocalization in UVB- or H₂O₂-stressed HaCaT human keratinocytes and HDF human dermal fibroblasts^[3].
PDRN (800 μg/mL; 24 h) upregulates the protein expression of SIRT1 and p62, downregulates LC3 levels, and reduces the expression of senescence markers p53 and p16 in UVB- or H₂O₂-stressed human keratinocyte HaCaT cells^[3].
PDRN (800 μg/mL; 24 h) downregulates the mRNA expression levels of senescence markers p53, p21, p16 and collagen-degrading enzyme MMP1 in UVB- or H₂O₂-stressed human keratinocyte HaCaT cells^[3].
PDRN (50-100 μg/mL) inhibits melanogenesis in a human melanocyte-keratinocyte co-culture system by targeting MITF, tyrosinase and TRP-1, accompanied by the phosphorylation of ERK and AKT^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.