| Abstrakt: |
Objective: Oxidative stress is considered a prime contributor to skin aging. Aged skin can be characterized by increased wrinkles and dry and dull appearance, which are associated with increased collagen degradation and inadequate desquamation, respectively. We investigated the antioxidant and skin anti-aging effects of a Ginkgo biloba leaf extract (GLE), an aqueous ethanol extract of Ginkgo biloba leaves, and the molecular mechanisms involved, using HaCaT keratinocytes. Methods: HaCaT cells were pretreated with GLE (0–15 μg/mL) and then treated with H2O2 (0.2 mM), and the cell viability and metalloproteinase 1 (MMP-1) protein level were measured. To investigate the mechanisms underlying the GLE's effects, the cells were incubated with GLE, and then glutathione content, cell migration rate, and the levels of proteins, i.e., MMPs, Kallikrein-related peptidases (KLKs), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), and mitogen-activated protein kinases, were measured. Results: GLE pretreatment caused decreases in cytotoxicity and the level of MMP-1, a key enzyme that degrades collagen in dermis, induced by H2O2 in HaCaT cells. GLE (5–15 μg/mL) caused increases in glutathione content and HO-1 level in cells, which appeared to be associated with the increase in Nrf2, a principal transcription factor for the antioxidant response. GLE also increased keratinocyte migration, which might result from the increase in KLK-7, a key enzyme that degrades corneodesmosomes and thus stimulates desquamation of corneocytes in epidermis. GLE increased the phosphorylation of c-Jun N-terminal protein kinase and extracellular signal-regulated kinase, which might contribute to the antioxidant and skin anti-aging effects of GLE demonstrated in our results. Conclusions: Our results suggest that GLE may have skin anti-aging effects by protecting keratinocytes against excessive oxidative stress via stimulation of antioxidant response, reducing wrinkle formation via a decrease in MMP-1 expression, and stimulating desquamation via an increase in KLK-7 expression. [ABSTRACT FROM AUTHOR] |
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