Comparative Evaluation of the Antioxidant Activity, and Anti-Melanogenic Properties of Diplotaxis tenuifolia and Eruca sativa Extracts on B16F10 Melanoma Cells

Hypermelanotic conditions including melasma, freckles and age spots occur largely due to the overproduction of melanin.Therefore, research has been increasingly focused on identification of melanogenesis inhibitors, especially among non-toxic, plant-derived compounds.The objective of this study was to assess and compare the antioxidative effects and the melanogenesis-suppressing potential of absolute ethanol extracts obtained from Diplotaxis tenuifolia (D. tenuifolia) and Eruca sativa (E.sativa).The antioxidative effects of the extracts were determined by measuring the total phenolic and flavonoid contents, along with a 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging assay.The suppression of mushroom-derived tyrosinase, cellular enzyme activity, as well as melanin content within B16F10 melanoma cells were examined to evaluate the anti-melanogenic effect.Both extracts dose-dependently inhibited mushroom tyrosinase, with D. tenuifolia achieving more than 50% reduction in enzyme activity, and a significant effect observed at 50 µg/mL (P<0.001),thus demonstrating a strong inhibitory effect on melanogenesis-related enzymatic processes.D. tenuifolia exhibited a marked suppressive effect on tyrosinase function and melanin synthesis within 3-isobutyl-1-methylxanthine-induced B16F10 melanoma cells, whereas the response elicited by E. sativa was notably less pronounced.Western blot analysis revealed that D. tenuifolia downregulated tyrosinase-related protein 1 (TRP-1) expression without altering microphthalmia-associated transcription factor (MITF) levels, suggesting the selective inhibition of melanin synthesis independent of MITF regulation.Notably, this effect was accompanied by a significant increase in phosphorylation of extracellular signal-regulated kinase (ERK), implying that activation of the ERK pathway may contribute to the post-transcriptional or post-translational suppression of TRP-1.