Eucommia ulmoides Bark Extract Attenuates Oxidative Damage and H2O2-Induced Hair Follicle Suppression in Cellular and Mouse Models
Xiaojin Liu, Shuyue Chen, Yanyan Zhang, Yaqian Qiu, Yefan GuOxidative stress contributes to hair follicle aging, melanocyte dysfunction, and androgen-related hair disorders, yet chemically characterized botanical interventions with multi-target activities remain incompletely defined. This study evaluated the antioxidant, follicle-supporting, and antiandrogenic potential of Eucommia ulmoides bark extract (EUE) using integrated in vitro and in vivo approaches and characterized EUE by HPLC-DAD using geniposidic acid and chlorogenic acid as representative marker compounds. Chlorogenic acid and geniposidic acid were present at 3.21 ± 0.01 and 1.88 ± 0.15 mg/g extract, respectively. In replicate-well assays using H2O2-challenged B16 melanoma cells, EUE increased superoxide dismutase activity and reduced malondialdehyde accumulation. Technical-triplicate RT-qPCR measurements and a single Western blot experiment showed descriptive changes in Nrf2 and HO-1 markers; these observations are exploratory and require independent biological replication. In HDPCs, replicate-well viability assays and technical-triplicate RT-qPCR measurements indicated concentration-associated viability changes and descriptive changes in VEGF, Wnt5a, and β-catenin transcripts. EUE also inhibited 5α-reductase activity in a cell-free assay, although the non-monotonic response and the much higher mass concentrations used relative to finasteride preclude potency equivalence. In male C57BL/6 mice, topical EUE attenuated H2O2-induced suppression of hair follicle elongation and improved follicular morphology. Overall, EUE is a chemically characterized botanical extract with preliminary biological activities relevant to oxidative stress- and androgen-associated hair disorders; independent replication, active-compound identification, marker-specific permeation, and protein-level validation of the measured markers remain necessary.