Radiofrequency irradiation attenuates angiogenesis and inflammation in UVB-induced rosacea in mouse skin

Rosacea is a skin inflammatory condition accompanied by cutaneous signs such as oedema, flushing, erythema, telangiectasia and pustules. Generally, rosacea is triggered by ultraviolet B (UVB) exposure. When exposed to UVB, skin epidermis thickens and produces elevated levels of pro-inflammatory cytokines, especially keratinocyte-related VEGF, a potent angiogenic factor. The upregulations of VEGF expression and its secretion promote the formation of new blood vessels and exacerbates rosacea. In this study, radiofrequency (RF) irradiation reduced keratinocyte proliferation in the epidermal layer, the expressions of pro-inflammatory cytokines, angiogenesis-related inflammatory factors and VEGF in our UVB-induced model of rosacea in vitro and in vivo. RF irradiation attenuated VEGF-induced angiogenesis-associated processes such as tube formation, cell migration and endothelial cell proliferation. Notably, blood vessel densities in the skins of UVB-treated mice and rosacea patients were significantly decreased by RF irradiation. These results provide experimental and molecular evidence regarding the effectiveness of RF irradiation for the treatment of rosacea.     

Melatonin compensates silencing of heat shock protein 70 and suppresses ultraviolet radiation‐induced inflammation in human skin ex vivo and cultured keratinocytes

Melatonin, a lipophilic compound synthesized and released from the pineal gland, effectively acts against ultraviolet radiation (UVR), one of the main inducers of epidermal damage, skin cancer, inflammation, and DNA photo damage. One of the common known stress protein induced by UVR is heat shock protein 70 (Hsp70), highly expressed in human keratinocytes, providing cellular resistance to such stressors. Here, using human full‐thickness skin and normal human epidermal keratinocytes (NHEK), we investigated the interaction of melatonin and Hsp70 toward UVR‐induced inflammatory and apoptotic responses. The following observations were made: (i) UVR upregulated Hsp70 gene expression in human epidermis while melatonin significantly inverted this effect, (ii) similar patterns of regulation were observed within Hsp70 protein level, and (iii) mechanistic studies involving silencing of Hsp70 RNA (Hsp70 siRNA) showed prominent decrease of IκB‐α (an inhibitor of NF‐κB) and enhanced gene expression of pro‐inflammatory cytokines (IL‐1β, IL‐6, Casp‐1) and pro‐apoptotic protein (Casp‐3) in NHEK. Parallel investigation using melatonin (10^?3 m ) significantly inverted these responses regardless depletion of Hsp70 RNA suggesting a compensatory action of this compound in the defense mechanisms. Our findings combined with data reported so far thus enrich existing knowledge about the potent anti‐apoptotic and anti‐inflammatory action of melatonin.     

Evaluation of ex vivo melanogenic response to UVB,UVA, and visible light in facial melasma and unaffected adjacent skin

BackgroundThe independent role of solar radiation in the differential melanogenesis between melasma and adjacent skin is unknown.ObjectivesTo assess the melanogenic responses of skin with facial melasma and of the adjacent skin to UVB, UVA, and visible light, in an ex vivo model.MethodsThis was a quasi-experimental study involving 22 patients with melasma. Facial melasma and adjacent skin samples were collected and stored in DMEM medium, at room temperature. One fragment was placed under the protection from light, while another was exposed to UVB, UVA, and visible light (blue-violet component): 166 mJ/cm², 1.524 J/cm², and 40 J/cm², respectively. Subsequently, all samples were kept for 72 hours in a dark environment and stained by Fontana-Masson to assess basal layer pigmentation, dendrites, and melanin granulation.ResultsEffective melanogenesis was observed in the basal layer in melasma and in the normal adjacent skin after all irradiations (p < 0.01), with the following median increment: UVB (4.7% vs. 8.5%), UVA (9.5% vs. 9.9%), and visible light (6.8% vs. 11.7%), with no significant difference between anatomical sites. An increase in melanin granulation (coarser melanosomes) was observed only after irradiation with UVA and only in the skin with melasma (p = 0.05). An increase in the melanocyte dendrite count induced by UVB radiation was observed in both anatomical sites (p ≤ 0.05).Study limitationsUse of an ex vivo model, with independent irradiation regimes for UVB, UVA, and visible light.ConclusionsMelanogenesis induced by UVB, UVA, and visible light was observed both in melasma and in the adjacent skin. The morphological patterns suggest that different irradiations promote individualized responses on the skin with melasma.     

Dosis eritematosa mínima: correlación con el fototipo y método de medición en una muestra de población colombiana

Background and objectiveThe minimal erythema dose (MED), an essential measurement in studies of skin photosensitivity, requires establishing MED values for specific populations, given genetic variation. Different ways to assess erythema are also relevant. We aimed to determine MED values in a sample of Colombian patients and correlations between MED and Fitzpatrick skin type. We also studied concordance correlation between MEDs and two alternative ways to assess erythema.Patients and methodsCross-sectional study of 113 individuals in Bogotá, Colombia. We used a solar simulator to measure UV-A radiation and combined UV-A and UV-B (UVA + UVB) radiation, o se podría suprimir este término porque UVA y UVB son términos conocidos for MED calculation. Narrowband UV-B (NBUVB) radiation was measured in a phototherapy cabin. Erythema was assessed visually and with a Mexameter MX 18 device.ResultsThe median MEDs of UVA + UVB radiation were 22 mJ/cm² for Fitzpatrick skin types I and II, and 33 and 43 mJ/cm², respectively, for types III and IV. The MEDs of UV-A radiation were 22, 42, 86, and 100 J/cm² for types I, II, III, and IV, respectively. The MEDs of NBUVB light were 390, 550, 770, and 885 mJ/cm² for the 4 skin types. The correlation between MEDs and skin types ranged from 0.5 to 0.69. Lin's concordance correlation coefficients between visual and Mexameter assessments of erythema were greater than 0.8 in all cases.ConclusionThis study allowed us to understand MED values for UV-A, UVA + UVB, and NBUVB according to different skin types in the Colombian population. Concordance correlation coefficients between the different methods of erythema assessment were very good. Correlations between MEDs and skin types were moderate to good.     

外源性胆绿素对中波紫外线诱导的角质形成细胞光损伤的保护作用和机制

【摘要】 目的 探讨外源性胆绿素对中波紫外线（UVB）照射的HaCaT细胞光损伤的保护作用。方法 将HaCaT细胞分为加入0、0.1、1、10 μmol/L胆绿素并照射UVB的UVB组、0.1 μmol/L UVB组、1 μmol/L UVB组、10 μmol/L UVB组及不做处理的对照组。UVB照射剂量为30 mJ/cm2，照射后继续培养24 h，分别检测细胞活性氧（ROS）水平、超氧化物歧化酶（SOD）活力、丙二醛（MDA）含量，ELISA法检测各组细胞的炎症因子白细胞介素6（IL-6）、IL-8水平。多组间均数比较采用单因素方差分析，组间两两比较采用LSD-t检验。结果 UVB组、0.1 μmol/L UVB 组、1 μmol/L UVB组、10 μmol/L UVB组、对照组细胞ROS水平（3 613.33 ± 206.61、2 958.67 ± 193.87、2 678.33 ± 178.24、2 274.67 ± 118.81、1 905.67 ± 250.25）、SOD活力（24.41 ± 1.78、28.96 ± 2.21、29.75 ± 1.75、30.19 ± 2.29、37.52 ± 2.31）、MDA含量（5.61 ± 0.32、5.46 ± 0.55、4.65 ± 0.22、2.55 ± 0.93、1.31 ± 0.05）、IL-6水平、IL-8水平差异均有统计学意义（F值分别为 34.02、57.36、214.09、29.73、11.40，均P < 0.05），UVB组ROS水平、MDA含量及IL-6、IL-8水平均高于另4组（均P < 0.05），SOD活力均低于另4组（均P < 0.05）。结论 外源性胆绿素减轻UVB引起的HaCaT细胞的氧化损伤、减轻炎症反应和抑制脂质过氧化作用，对细胞光损伤有一定的保护作用。     

窄谱中波紫外线治疗白癜风治疗参数选择

【摘要】 我国窄谱中波紫外线应用于白癜风治疗已有十余年，目前，其临床治疗参数尚缺乏统一标准，不规范的治疗不仅不能使患者从中获益，还易引起红斑、水疱、光老化等不良反应。基于世界白癜风工作组光疗委员会制定的窄谱中波紫外线治疗白癜风的专家共识，结合相关文献及临床治疗经验，本文从治疗频率、初始治疗剂量、连续治疗或中断治疗后剂量调整、平台期及疗程选择、可接受的最大光疗总次数等方面讨论窄谱中波紫外线治疗参数的选择，提高窄谱中波紫外线治疗白癜风的疗效。     

Relationship between lifespan and somatic mutation in D. melanogaster after treatment with chlorophyllin

Sodium copper chlorophyllin (SCC) has a genetic damage inhibitory capacity due to its antioxidant action. For this reason, it was considered to investigate its role in the life span of Drosophila melanogaster and its relationship with the frequency of somatic mutation induced by gamma rays. Results indicated that SCC alone prolonged the lifespan only in females, but in combination with 20 Gy of gamma rays, the aging delay in both sexes was significant. In addition to confirming that the porphyrin reduces the frequency of mutation, the individuals with the highest mutation load are the individuals who die more quickly, and once they are eliminated, the survivor individuals treated with 20 Gy or with SCC + 20 Gy, died at the same rate. The results together indicate that SCC not only inhibits induced genetic damage, but it also has beneficial effects that probably cause an aging delay of the treated population that need to be investigated.