Abstract
Ultraviolet-B (UVB) exposure is one of the primary extrinsic factors causing skin photoaging. It stimulates inflammatory responses and arrests the cell cycle. Matrix metalloproteinase-1 (MMP-1) secreted by keratinocytes is one of the important extracellular matrixes to attenuate UVB-induced skin aging via collagen degradation. Curcuma aromatica (CA) and Curcuma comosa (CC), the herbaceous plants in the Zingiberaceae family, are commonly used in Thai traditional women’s medicines. The present work was aimed to investigate the potential of the CA and CC extracts and their isolated compounds to attenuate UVB-induced MMP-1 and cell cycle arrest in HaCaT keratinocytes. Total phenolic contents and antioxidant capacities of the extracts were determined. CC extract contains more phenolic components and provides more potent antioxidant activities than CA extract. HaCaTs were pretreated with the extracts or their isolated constituents 1–4 for 24 h and then repeatedly exposed to UVB at 100 mJ/cm2 10 times. Both extracts and compounds 1–4 effectively reduce UVB-induced MMP-1 levels in HaCaT cells and restore cell cycle arrest. This is the first report on the potential of CA and CC extracts in reducing UVB-induced MMP-1 expression and regulating cell proliferation in HaCaT cells. Thus, CA and CC extracts might be used as alternative natural agents to prevent UVB-induced skin photoaging.
Highlights
Skin aging is a complicated biological process affected by both intrinsic and extrinsic influences
In preliminary screening for anti-photoaging agents, it was found that the ethanolic extracts of Curcuma aromatica (CA) and Curcuma comosa (CC) exerted cytoprotective activity against UVB irradiation in human HaCaT keratinocytes by inducing the expression of Matrix metalloproteinase-1 (MMP-1)
The results were expressed as mean ± standard deviation (SD) of triplicate experiments. (n = 3) 1 L-Ascorbic acid was used as the positive control
Summary
Skin aging is a complicated biological process affected by both intrinsic and extrinsic influences. UVB is responsible for the majority of UV radiation that directly penetrates the skin, which causes skin pigmentation and wrinkles, as well as inducing the synthesis of activator protein-1 (AP-1), activating nuclear factor kappa-light-chainenhancer of activated B cells (NF-κB), generating reactive oxygen species (ROS) on cell surface receptors, such mitogen-activated kinases (MAPK) stimulating the induction and the expression of matrix metalloproteinases (MMPs) [8]. Because of this damage it is well-established that UVB is more genotoxic than UVA. Collagen breakdown and degradation are hallmarks of photoaging, so an increase in MMP-1 expression or activity is an indication of UV-induced skin damage [11,12,13,14]
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