Abstract
The skin of an organism is affected by various environmental factors and fights against aging stress via mechanical and biochemical responses. Photoaging induced by ultraviolet B (UVB) irradiation is common and is the most vital factor in the senescence phenotype of skin, and so, suppression of UVB stress-induced damage is critical. To lessen the UVB-induced hyperimmune response and hyperpigmentation, we investigated the ameliorative effects of intense pulsed light (IPL) treatment on the photoaged phenotype of skin cells. Normal human epidermal keratinocytes and human epidermal melanocytes were exposed to 20 mJ/cm2 of UVB. After UVB irradiation, the cells were treated with green (525–530 nm) and yellow (585–592 nm) IPL at various time points prior to the harvest step. Subsequently, various signs of excessive immune response, including expression of proinflammatory and melanogenic genes and proteins, cellular oxidative stress level, and antioxidative enzyme activity, were examined. We found that IPL treatment reduced excessive cutaneous immune reactions by suppressing UVB-induced proinflammatory cytokine expression. IPL treatment prevented hyperpigmentation, and combined treatment with green and yellow IPL synergistically attenuated both processes. IPL treatment may exert protective effects against UVB injury in skin cells by attenuating inflammatory cytokine and melanogenic gene overexpression, possibly by reducing intracellular oxidative stress. IPL treatment also preserves antioxidative enzyme activity under UVB irradiation. This study suggests that IPL treatment is a useful strategy against photoaging, and provides evidence supporting clinical approaches with non-invasive light therapy.
Highlights
Published: 20 March 2021The skin functions as the outermost organ and a defense barrier in the body
ultraviolet B (UVB)-induced photoaging is an explicit example of aging stress, as indicated by comparisons between photoexposed and photoprotected skin; such comparisons have revealed that genes related to deoxyribonucleic acid (DNA) repair and replication, chromatin remodeling, oxidative stress responses, autophagy, protein metabolism, and cell growth and survival are differentially expressed in youthful skin compared with photoaged skin [2]
We found that intense pulsed light (IPL) treatment reduced the expression of the melanogenic proteins MITF, TYR, tyrosinase-related protein 1 microphthalmia-associated (TYRP1), dopachrome tautomerase (DCT), stem cell factor (SCF), and SOX10, which are involved in UV-induced hyperpigmentation (Figure 5B)
Summary
Published: 20 March 2021The skin functions as the outermost organ and a defense barrier in the body. Aging stress in the skin is provoked mainly by ultraviolet B (UVB) irradiation. UVB-induced photoaging is an explicit example of aging stress, as indicated by comparisons between photoexposed (face and arm) and photoprotected (buttocks) skin; such comparisons have revealed that genes related to deoxyribonucleic acid (DNA) repair and replication, chromatin remodeling, oxidative stress responses, autophagy, protein metabolism, and cell growth and survival are differentially expressed in youthful skin compared with photoaged skin [2]. UVB light is absorbed by DNA and induces direct DNA damage, causes oxidative stress, and upregulates transcription factors [3]. UVB exposure elevates the generation of a variety of inflammatory cytokines and diverse genes associated with DNA repair, oxidative stress responses, protein metabolism, and immune responses. In some instances, accumulated damage caused by acute or spontaneous UVB exposure leads to a hyperimmune reaction in skin
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