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BackgroundExcessive exposure of the skin to UV radiation (UVR) triggers a remodeling of the immune system and leads to the photoaging state which is reminiscent of chronological aging. Over 30 years ago, it was observed that UVR induced an immunosuppressive state which inhibited skin contact hypersensitivity.MethodsOriginal and review articles encompassing inflammation and immunosuppression in the photoaging and chronological aging processes were examined from major databases including PubMed, Scopus, and Google Scholar.ResultsCurrently it is known that UVR treatment can trigger a cellular senescence and inflammatory state in the skin. Chronic low-grade inflammation stimulates a counteracting immunosuppression involving an expansion of immunosuppressive cells, e.g., regulatory T cells (Treg), myeloid-derived suppressor cells (MDSC), and regulatory dendritic cells (DCreg). This increased immunosuppressive activity not only suppresses the function of effector immune cells, a state called immunosenescence, but it also induces bystander degeneration of neighboring cells. Interestingly, the chronological aging process also involves an accumulation of pro-inflammatory senescent cells and signs of chronic low-grade inflammation, called inflammaging. There is also clear evidence that inflammaging is associated with an increase in anti-inflammatory and immunosuppressive activities which promote immunosenescence.ConclusionIt seems that photoaging and normal aging evoke similar processes driven by the remodeling of the immune system. However, it is likely that there are different molecular mechanisms inducing inflammation and immunosuppression in the accelerated photoaging and the chronological aging processes.

[Display omitted] The association of sunrays with skin damage have been known since medieval times. The description of the electromagnetic spectrum facilitated the identification of the ultraviolet light spectrum as being responsible for skin damage resulting from prolonged skin exposure. Sunscreens have been used since ancient civilizations with various measures to limit exposure to sun exposure being employed. Awareness of the risks associated with sunrays has been increasing in the last century, and as a result, the science, technologies, and formulation have advanced significantly. The use of sunscreen products continues rising as government health agencies seek to contain increasing cases of UV induced melanomas. Recreational sunbathing and artificial tanning have increased the risk for these diseases significantly. This review article sought to expound the scientific basis of sunscreen use, the classification, formulation, quality control and regulation across the different countries around the world. The literature review was conducted on Google scholar, PubMed, SCOPUS, Cochrane, BMJ, SCIELO among others.

Ultraviolet (UV) radiation is a major cause of photoaging that can induce DNA damage, oxidative stress, and cellular aging. Metformin (MF) can repair DNA damage, scavenge reactive oxygen species (ROS), and protect cells. However, the mechanism by which MF inhibits cell senescence in chronic skin damage induced by UVA is unclear. In this study, human foreskin fibroblasts (HFFs) treated with UVA were used as an in vitro model and UVA-induced skin photoaging in Kunming mice was used as an in vivo model to investigate the potential skin protective mechanism of MF. The results revealed that MF treatment attenuated UVA-induced cell viability, skin aging, and activation of the PI3K/AKT/mTOR signaling pathway. Furthermore, MF treatment alleviated the mitochondrial oxidative stress and decreased mitophagy. Knockdown of Parkin by siRNA increased the clearance of MF in senescent cells. The treatment of Kunming mice with MF at a dose of 10 mg/kg/day significantly reduced UVA-induced skin roughness, epidermal thinning, collagen degradation, and skin aging. In conclusion, our experimental results suggest that MF exerts anti-photoaging effects by inhibiting mitophagy and the PI3K/AKT/mTOR signaling pathway. Therefore, our study improves the current understanding of the protective mechanism of MF against photoaging.

Skin aging is categorized as chronological aging and photo-aging that affected by intrinsic and extrinsic factors. The present study aimed to investigate the anti-aging ability and its underlying mechanism of chlorogenic acid (CGA) on human dermal fibroblasts (HDFs). In this study, CGA specifically up-regulated collagen I (Col1) mRNA and protein expressions and increased the collagen secretion in the supernatant of HDFs without affecting the cell viability, the latter was also demonstrated in BioMAP HDF3CGF system. Under ultraviolet A (UVA)-induced photoaging, CGA regulated collagen metabolism by increasing Col1 expression and decreasing matrix metalloproteinase 1 (MMP1) and MMP3 levels in UVA-irradiated HDFs. The activation of transforming growth factor-β (TGF-β)-mediated Smad2/3 molecules, which is crucial in Col1 synthesis, was suppressed by UVA irradiation and but enhanced at the presence of CGA. In addition, CGA reduced the accumulation of UVA-induced reactive oxygen species (ROS), attenuated the DNA damage and promoted cell repair, resulting in reducing the apoptosis of UVA-irradiated HDFs. In conclusion, our study, for the first time, demonstrate that CGA has protective effects during skin photoaging, especially triggered by UVA-irradiation, and provide rationales for further investigation of CGA being used to prevent or treat skin aging.

Background: Melasma is a challenging hyperpigmentation disorder without absolute treatment. Aims: This study aimed to evaluate the effects of intradermal botulinum toxin A (BoNT‐A) on melasma and the protective effects of BoNT‐A on UVA‐induced melanogenesis in B16F10 melanoma cells. Patients/Methods: This study is a split‐face randomized, double‐blind, placebo‐controlled trial in 12 melasma patients who received intradermal abobotulinumtoxinA injection into melasma lesions. An in vitro study was also conducted in B16F10 melanoma cells treated with different concentrations of BoNT‐A prior to exposure to UVA. Cell viability and cellular melanogenesis were determined. Results: The adjusted MASI scores on the BoNT‐A side were significantly lower than the control at 3 months after injection, 2.8 versus 4.5 ( p < 0.001), respectively. BoNT‐A injection significantly reduced the MASI score at 2 and 3 months compared with the baseline of 4.1–3.2 (22%) ( p < 0.001) and 2.8 (31.7%) ( p < 0.001), respectively. Melanin content and tyrosinase activity in B16F10 cells with or without UVA irradiation were significantly reduced by treatment with BoNT‐A in a dose‐dependent manner without causing cytotoxicity. Conclusions: BoNT‐A has a potentially beneficial effect in the treatment of melasma due to its antimelanogenic effect. Trial Registration: Clinical Trial Registry identifier: TCTR20250118001

Understanding the wavelength dependence of plant responses is essential for optimizing production and quality of indoor plant cultivation. UVA is the main component of solar UV radiation, but its role on plant growth is poorly understood. Here, two experiments were conducted to examine whether UVA supplementation is beneficial for indoor plant cultivation. Lettuce ( L. cv. \"Klee\") was grown under mixed blue, red, and far-red light with photon flux density of 237 μmol m s in the growth room; photoperiod was 16 h. In the first experiment, three UVA intensities with peak wavelengths at 365 nm were used: 10 (UVA-10), 20 (UVA-20), and 30 (UVA-30) μmol m s , respectively. In the second experiment, 10 μmol m s UVA radiation were given for 5 (UVA-5d), 10 (UVA-10d), and 15 (UVA-15d) days before harvest on day 15, respectively. Compared with control (no UVA), shoot dry weight was increased by 27%, 29%, and 15% in the UVA-10, UVA-20, and UVA-30 treatments, respectively, which correlated with 31% (UVA-10), 32% (UVA-20), and 14% (UVA-30) larger leaf area. Shoot dry weight under the treatments of UVA-5d, UVA-10d, and UVA-15d was increased by 18%, 32%, and 30%, respectively, and leaf area was increased by 15%-26%. For both experiments, UVA radiation substantially enhanced secondary metabolites accumulation, e.g. anthocyanin and ascorbic acid contents were increased by 17%-49% and 47%-80%, respectively. Moreover, plants grown under the UVA-30 treatment were stressed, as indicated by lipid peroxidation and lower maximum quantum efficiency of photosystem II photochemistry (F /F ). We conclude that UVA supplementation not only stimulates biomass production in controlled environments, but also enhances secondary metabolite accumulation.

Different wavelengths of ultraviolet (UV) light cause skin damage through different mechanisms. Minimal erythema dose (MED) is usually used to clinically evaluate skin sensitivity to ultraviolet radiation by inducing skin erythema using ultraviolet B (UVB) or ultraviolet A (UVA) + UVB. In this study, we detected changes in the blood flow at the MED erythema caused by UVB and UVA + UVB radiation through optical coherence tomography (OCT) to explain the role of different bands of ultraviolet rays in erythema induction. Two MED irradiation areas on the subjects' back were irradiated with UVB alone or UVA + UVB (UVA: UVB = 8:1). The absolute energy of UVB remained the same in UVB and UVA+UVB. At 24 h after the irradiation, the changes in the blood flow in the MED area were detected using OCT. Compared with the blank control, the maximum blood flow depth, blood flow peak, and total blood flow of UVB-MED and UVA+UVB-MED were significantly increased. Notably, the maximum blood flow depth and blood flow peak of UVB-MED were higher than UVA+UVB-MED. There was no significant difference in total blood perfusion between UVA+UVB-MED and UVB-MED. Under the same UVB energy, the skin erythema caused by UVA + UVB was weaker than UVB alone. The analysis of local blood flow by OCT showed that the peak and maximum depth of local blood flow caused by UVB alone were significantly higher than UVA + UVB.

Broccoli sprouts contain health-promoting phytochemicals that can be enhanced by applying ultraviolet light (UV) or phytohormones. The separate and combined effects of methyl jasmonate (MJ), UVA, or UVB lights on glucosinolate, phenolic, carotenoid, and chlorophyll profiles were assessed in broccoli sprouts. Seven-day-old broccoli sprouts were exposed to UVA (9.47 W/m2) or UVB (7.16 W/m2) radiation for 120 min alone or in combination with a 25 µM MJ solution, also applied to sprouts without UV supplementation. UVA + MJ and UVB + MJ treatments increased the total glucosinolate content by ~154% and ~148%, respectively. MJ induced the biosynthesis of indole glucosinolates, especially neoglucobrassicin (~538%), showing a synergistic effect with UVA stress. UVB increased the content of aliphatic and indole glucosinolates, such as glucoraphanin (~78%) and 4-methoxy-glucobrassicin (~177%). UVA increased several phenolics such as gallic acid (~57%) and a kaempferol glucoside (~25.4%). MJ treatment decreased most phenolic levels but greatly induced accumulation of 5-sinapoylquinic acid (~239%). MJ treatments also reduced carotenoid and chlorophyll content, while UVA increased lutein (~23%), chlorophyll b (~31%), neoxanthin (~34%), and chlorophyll a (~67%). Results indicated that UV- and/or MJ-treated broccoli sprouts redirect the carbon flux to the biosynthesis of specific glucosinolates, phenolics, carotenoids, and chlorophylls depending on the type of stress applied.

There are obvious drawbacks for the traditional treatment methods of antibiotics, such as low efficiency and high cost. In this paper, FeOx catalysts, modified with the biochar (BC) of maple leaf (FeOx@BC), were successfully prepared by the hydrothermal method. Then, the FeOx@BC was investigated to activate peroxymonosulfate (PMS) under UVA-LED irradiation for the degradation of tetracycline hydrochloride (TC). Subsequently, the changes in valence states before and after the reaction of ions were investigated by XPS spectra, and the process mechanism was presented. The results demonstrated that the TC degradation efficiency reached 96% in the FeOx@BC + PMS + UVA-LED system within 40 min, which was higher than 57% efficiency for the α-Fe2O3 + PMS + UVA-LED system. The electron transfer was promoted in the FeOx@BC + PMS + UVA-LED system due to the doping of BC. The Fe(III) was transformed into Fe(II) under UVA-LED irradiation, and Fe(II) activated continuously PMS to generate active oxygen species. Furthermore, it had excellent reusable performance and structural stability, and the degradation efficiency was still as high as 80% after five cycles. It was proved that SO4−•, •OH, O2•− and h+ participated in the degradation process of TC to different degrees by quenching experiments and EPR tests. In summary, FeOx@BC is an inexpensive, reusable and efficient catalyst.

Grape seed powder (GSP), grape skin powder (GSKP), or grape pomace powder (GPP) was introduced as partial substitution for wheat flour (WF) with variable percentages by weight (0- 20 wt%), and the resultant addition effects on the rheological and microstructural properties were studied. GPP and GSP significantly (p < .05) reduced the water absorption but three types of grape powders could increase the development time and dough stability. Furthermore, all kinds of grape powders with various incorporations could significantly (p < .05) enhance the strength of dough systems. Grape powders decreased the storage (G′) and loss (G″) moduli, while the tan δ increased with the increasing of GSP/GSKP/GPP addition levels. The microstructure observation of composite doughs suggested that the integrity and continuity of gluten networks were destroyed in the presence of grape powders. Based on the above results, the GSP addition levels of 10% to 15%, GSKP/GPP of 5% to 10% are recommended.