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.     

UV radiation induces CXCL5 expression in human skin

CXCL5 has recently been identified as a mediator of UVB‐induced pain in rodents. To compare and to extend previous knowledge of cutaneous CXCL5 regulation, we performed a comprehensive study on the effects of UV radiation on CXCL5 regulation in human skin. Our results show a dose‐dependent increase in CXCL5 protein in human skin after UV radiation. CXCL5 can be released by different cell types in the skin. We presumed that, in addition to immune cells, non‐immune skin cells also contribute to UV‐induced increase in CXCL5 protein. Analysis of monocultured dermal fibroblasts and keratinocytes revealed that only fibroblasts but not keratinocytes displayed up regulated CXCL5 levels after UV stimulation. Whereas UV treatment of human skin equivalents, induced epidermal CXCL5 mRNA and protein expression. Up regulation of epidermal CXCL5 was independent of keratinocyte differentiation and keratinocyte‐keratinocyte interactions in epidermal layers. Our findings provide first evidence on the release of CXCL5 in UV‐radiated human skin and the essential role of fibroblast‐keratinocyte interaction in the regulation of epidermal CXCL5.     

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.     

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。     

窄谱中波紫外线治疗对寻常型银屑病Th22细胞及其相关细胞因子表达的影响

目的:观察窄谱中波紫外线(NB-UVB)治疗寻常型银屑病的疗效以及对寻常型银屑病患者Th22细胞及相关细胞因子的影响,探讨NB-UVB治疗银屑病的作用机制。方法:40例寻常型银屑病患者NB-UVB治疗20次,以皮损面积和严重程度(PASI)评分评价疗效;取患者治疗前后的外周血,用三色法流式细胞仪检测Th22细胞,ELISA法检测IL-6及IL-22的水平,并与健康对照组进行比较。结果:NB-UVB治疗后PASI评分明显下降(P0.01);银屑病患者治疗前外周血Th22、IL-6及IL-22的水平较对照组均明显增高(P0.01)。治疗后外周血Th22细胞的百分比(1.19±0.31)%,血清IL-6的水平(15.27±1.66)pg/mL及IL-22的水平(38.52±3.31)pg/mL较治疗前均明显下降(P值均0.01),且三者水平高低均与PASI呈正相关(P值均0.05)。结论:NB-UVB可能通过影响Th22细胞及IL-6、IL-22细胞因子来发挥治疗银屑病的作用。