Abstract
Ultraviolet (UV) radiation induces skin photoaging, which is associated with the elevation of matrix metalloproteinases (MMPs) and the impairment of collagen. The Euphrasia species play a well-known role in the treatment of certain eye disorders through their anti-oxidative and anti-inflammatory activities. However, their protective activity toward UVB-induced damage remains unclear. In the present study, we investigated the protective effect of Euphrasia officinalis (95% ethanol extract) on UVB-irradiated photoaging in normal human dermal fibroblasts (NHDFs). Our results show that Euphrasia officinalis extract exhibited obvious reactive oxygen species (ROS) and 2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging activity, enhanced NHDF cell migration, and reduced UVB-induced apoptosis. The UVB-induced increases in MMP-1 and MMP-3 and decrease in type I procollagen were ameliorated by Euphrasia officinalis treatment, which worked by suppressing the mitogen-activated protein kinase (MAPK) and nuclear transcription factor activator protein 1 (AP-1) signaling pathways. Taken together, our data strongly suggest that Euphrasia officinalis ethanol extract could reduce UVB-induced photoaging by alleviating oxidative stress, proinflammatory activity, and cell apoptosis.
Highlights
Skin aging is a complex process that is affected by both intrinsic factors such as genetics, hormonal changes, and metabolic processes and extrinsic factors such as solar radiation, smoking, pollution, and chemical exposure [1,2]
Severe and chronic UVB irradiation causes photoaging by the production of excessive intracellular reactive oxygen species (ROS); this results in oxidative stress, which is an important mediator of damage to cell structures [7]
normal human dermal fibroblasts (NHDFs) were exposed to UVB irradiation (144 mJ/cm2) and treated with E. officinalis (1 μg/mL, 10 μg/mL, or 50 μg/mL)
Summary
Skin aging is a complex process that is affected by both intrinsic factors such as genetics, hormonal changes, and metabolic processes and extrinsic factors such as solar radiation, smoking, pollution, and chemical exposure [1,2]. Solar ultraviolet (UV) radiation is a major extrinsic photoaging factor that is divided into three categories: UVA (315–400 nm), UVB (280–315 nm), and UVC (100–280 nm). UVB-induced ROS generation activates the mitogen-activated protein kinase (MAPK) signaling pathway [8]. MAPK activation upregulates the transcription of activator protein 1 (AP-1), which induces matrix metalloproteinase (MMP) expression and collagen degradation. MMP-1, an interstitial collagenase or fibroblast collagenase, degrades transforming growth factor-β1 (TGF-β1), collagen, and elastin in the extracellular matrix (ECM) [10]. An increase in IL-6 leads to collagen degradation by accelerating fibroblast and MMP expression and cell apoptosis
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