Abstract
While harmful effects of blue light on skin cells have been recently reported, there are few studies regarding natural products that alleviate its negative effects. Therefore, we investigated ameliorating effects of yellow chaste weed (YCW) (Helichrysum arenarium) extract and its components, apigenin and galangin, on blue light-irradiated HaCaT cells. In this study, we found that YCW extract improved the reduced proliferation of HaCaT cells induced by blue light-irradiation and reduced blue light-induced production of reactive oxygen species (ROS) levels. We also found that apigenin and galangin, the main components of YCW extract, showed the same activities as YCW extract. In experiments examining molecular mechanisms of YCW extract and its components such as apigenin and galangin, they all reduced expression of transient receptor potential vanilloid member 1 (TRPV1), its phosphorylation, and calcium ion (Ca2+) influx induced by blue light irradiation. In addition, apigenin and galangin regulated phosphorylation of mitogen-activated protein kinases (MAPKs). They also reduced phosphorylation of mammalian sterile 20-like kinase-1/2 (MST-1/2), inducing phosphorylation of Akt (protein kinase B), one downstream molecule of MST-1/2. Moreover, apigenin and galangin promoted translocation of Forkhead box O3 (FoxO3a) from the nucleus to the cytosol by phosphorylating FoxO3a. Besides, apigenin and galangin interrupted blue light influences on expression of nuclear and secretory clusterin. Namely, they attenuated both upregulation of nuclear clusterin and downregulation of secretory clusterin induced by blue light irradiation. We also found that they downregulated apoptotic protein Bcl-2 associated X protein (Bax) and conversely upregulated anti-apoptotic protein B-cell lymphoma 2 (Bcl-2). Collectively, these findings indicate that YCW extract and its components, apigenin and galangin, antagonize the blue light-induced damage to the keratinocytes by regulating TRPV1/clusterin/FoxO3a and MAPK signaling.
Highlights
The skin is located at the outermost part of the human body, protecting us from a variety of external factors, including sun light, pollutants, and stresses
In our previous report, we demonstrated that the effects of blue light on keratinocyte cell proliferation are mediated by upregulating transient receptor potential vanilloid member 1 (TRPV1), a negative regulator of EGFR-FoxO3a signaling [10]
HaCaT cells were treated with various concentrations of yellow chaste weed (YCW) extract (0.01, 0.05, 0.1%) or apigenin (10, 20, 30 μM) or galangin (1, 10, 20 μM) or vehicle (DMSO) for 24 h in phenol red-free culture medium (PRFCM) before blue light irradiation
Summary
The skin is located at the outermost part of the human body, protecting us from a variety of external factors, including sun light, pollutants, and stresses. These various external factors induce many physiological changes in skin, such as aging, pigmentation/vitiligo, skin inflammation, and hair loss. One of the biggest factors affecting the skin, is largely composed of ultraviolet (UV), visible and infrared light, depending on energy and wavelength [5,6]. Excessive exposure to blue light has been reported to induce several damages to skin cells, including oxidative stress, apoptosis, and reduced proliferation potential [9,10]. Blue light induces several damages to the epidermis, including DNA damage and oxidative stress [11–13]
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