日光对皮肤弹性的影响

目的观察日光和年龄对皮肤弹性的影响。方法问卷调查受试者（郊县组94例，市区组105例）的日光曝晒情况，并应用皮肤弹性测量仪测量外眦部、鼻唇沟及眶下皮肤弹性参数，包括：弹性，黏弹性，可扩展性和张力参数。比较不同年龄组间、市区与郊县组间各弹性参数间的差异。结果市区和郊县各弹性参数均与年龄有较好的相关性，随年龄增长，皮肤各弹性参数均下降。郊县组与市区组比较，弹性和黏弹性参数差异较小，而可扩展性和张力参数差异较大。结论弹性和黏弹性参数可能与内在老化有关，而可扩展性和张力参数可能与光老化有关。     

灯盏花素灌胃对紫外线致SD大鼠皮肤光老化的保护作用

目的探讨灯盏花素抗光老化的作用机制,为防治光老化性疾病提供实验依据。方法 SD大鼠随机分成6组,正常对照组(A组)、模型对照组(B组)、模型+维生素E30mg/kg对照组(C组)、模型+灯盏花素35mg/kg低剂量组(D组)、模型+灯盏花素70mg/kg中剂量组(E组)、模型+灯盏花素140mg/kg高剂量组(F组),模拟日光中UV(UVA+UVB)长期照射,造成皮肤光老化模型。观察皮肤的肉眼改变、组织结构改变及核转录因子κB(NF-κB)和增殖细胞核抗原(PCNA)在大鼠皮肤中的表达与分布情况。结果 E组、F组大鼠皮肤红斑、脱屑、皱纹等光老化改变明显比B组轻;D组、E组、F组皮肤光老化病理改变逐渐减轻;D组、E组、F组分别与B组比较,NF-κB和PCNA的表达均有所减少,D组与B组间比较及F组与E组间比较差异均无统计学意义(P>0.05)。结论 NF-κB,PCNA在光老化模型中的高表达提示两者可能与光老化的形成有关;灯盏花素可能通过抑制PCNA的表达,抑制表皮细胞的增殖及通过抑制NF-κB的活化,从而下调炎症介质的合成,发挥其抗皮肤光老化的作用。     

红光加类人胶原蛋白敷料对改善点阵 CO2激光治疗光老化皮肤术后色素沉着的效果观察

目的：探讨红光加类人胶原蛋白敷料对改善点阵 CO2激光治疗光老化皮肤术后色素沉着的临床效果。方法：选择患者80例,按照简单随机数字表法分为两组,各40例,对照组进行红光照射,观察组在对照组治疗基础上联合使用类人胶原蛋白敷料比较两组患者治疗前后 VISIA 皮肤图像分析仪、SOFT5．5皮肤性质测试仪测定结果,并统计两组治疗后优、良率及色素沉着治疗起效时间。结果：治疗后观察组色素斑、皱纹、纹理、毛孔及紫质评分均优于对照组,差异具有统计学意义（P＜0．05）,治疗后观察组 pH、水分、弹性及油脂评分均优于对照组,差异具有统计学意义（P＜0．05）,观察组治疗后优良率为90．0％,高于对照组的50．0％,差异具有统计学意义（P＜0．05）,观察组治疗后临床效果为优和良者起效时间快于对照组,差异具有统计学意义（P＜0．05）。结论：红光联合类人胶原蛋白敷料可改善点阵CO2激光治疗光老化皮肤术后皮肤弹性,增加皮肤水分,缩小毛孔,减少油脂分泌和皮肤色素沉着。     

Introduction to skin aging

Cutaneous science has seen considerable development in the last 25 years, in part due to the Omics revolution, and the appreciation that this organ is hardwired into the body's key neuro-immuno-endocrine axes. Moreover, there is greater appreciation of how stratification of skin disorders will permit more targeted and more effective treatments. Against this has been how the remarkable extension in the average human life-span, though in the West at least, this parallels worrying increases in lifestyle-associated conditions like diabetes, skin cancer etc. These demographic trends bring greater urgency to finding clinical solutions for numerous age-related deficits in skin function caused by extrinsic and intrinsic factors. Mechanisms for aging skin include the actions of reactive oxygen species (ROS), mtDNA mutations, and telomere shortening, as well as hormonal changes.We have also significantly improved our understanding of how to harness the skin's considerable regenerative capacity e.g., via its remarkable investment of stem cell subpopulations. In this way we hope to develop new strategies to selectively target the skin's capacity to undergo optimal wound repair and regeneration. Here, the unsung hero of the skin regenerative power may be the humble hair follicle, replete with its compliment of epithelial, mesenchymal, neural and other stem cells. This review introduces the topic of human skin aging, with a focus on how maintenance of function in this complex multi-cell type organ is key for retaining quality of life into old age.     

Expression of decorin and collagens I and III in different layers of human skin in vivo: a laser capture microdissection study

Extracellular matrix (ECM) organization is a complex process that requires the coordinated efforts of many molecules. For the regulation of collagen fiber diameter, the proteoglycan decorin appears to be of major relevance. To investigate the role of decorin in the process of (photo-)aging in more detail, full-thickness punch biopsies were isolated from human buttock skin. Single exposure with two minimal erythemal doses of solar simulated irradiation caused down-regulation of decorin mRNA in young (n = 5) and old subjects (n = 5) after 24 h. Interestingly, decorin mRNA was elevated with age. To test the hypothesis that a decreased collagen-to-decorin-ratio impairs collagen structure we also investigated collagens I and III gene expression. Both were down-regulated with increasing age and after single UV-irradiation. As determined by laser capture microdissection-quantitative real time-Polymerase chain reaction (n = 11), decorin is mostly present in the reticular dermis while being absent from the papillary dermis. Minor expression was also observed in the epidermis. However, in contrast to full-thickness skin biopsies age-dependent changes in collagens I, III, and decorin expression could not be observed with this methodology indicating technical limitations. Together with our finding that collagens I and III mRNA are similarly expressed in the reticular and papillary dermis and are down-regulated by UV, our studies support the idea of a major role of decorin in ECM organization. Altered expression of decorin mRNA in the different dermal strata and a decrease in the collagen-to-decorin ratio inflicted by both age and ultraviolet irradiation possibly affect collagen bundle diameter and subsequently the mechanical properties of human skin.     

Cutaneous injury following acute UV-B radiation in a mouse model: a pilot histological study

Abstract

Epidemiological and clinical studies have implicated solar ultraviolet (UV) radiation, especially the UV-B radiation (290–320 nm wavelengths) as the principal agent that elicits sunburn, transient inflammation, melanoma and non-melanoma cancer, and premature skin aging. The common form of skin damage described as ‘photoaging’ is caused by repeated sun exposures; it can induce epithelial deoxyribonucleic acid (DNA) damage, and alter the structure and function of dermal connective tissue and extracellular matrix. The present study was aimed to elucidate the effects of a single exposure of different doses of UV-B radiation on the dorsal skin in the hairless mouse. The histopathologic sequels of such exposures were analyzed by using common staining methods, immunohistochemistry, and histomorphometry. Single UV-B exposures seem to elicit dose-graded histological changes some of which have been described in experiments with chronic exposure in this species.     

Photoaging as a consequence of natural and therapeutic ultraviolet irradiation—studies on PUVA-induced senescence-like growth arrest of human dermal fibroblasts

Premature aging of the skin is a prominent side effect of psoralen photoactivation, a therapy widely and successfully used for different skin disorders. Recently, we demonstrated that treatment of fibroblasts with 8-methoxypsoralen and ultraviolet A irradiation resulted in growth arrest with morphological and functional changes reminiscent of replicative senescence. In this minireview we will focus on the similarities between intrinsic and extrinsic aging and PUVA-induced senescence-like growth arrest both resulting in the loss of the structural integrity of the dermal connective tissue as a hallmark of intrinsic aging and photoaging (extrinsic aging) of the skin, and we will discuss the important role of oxidative stress related telomere attrition in the PUVA-induced phenotype of dermal fibroblasts.With the PUVA-induced growth arrest of fibroblasts a new model has been added to the growing number of in vitro models with longterm growth arrest upon exposure to sublethal stressors (i.e. hyperoxia, hydrogen peroxide, ethanol), which are characterized by morphological and functional changes common for cellular senescence. This model may be particularly suited for further studies addressing mechanisms of stress-induced senescence-like growth arrest in vitro and in vivo, since many dermatological patients are treated with PUVA allowing the analysis of putative stress-induced premature senescence in vivo.     

烟酰胺对光老化皮肤真皮羟脯氨酸含量的影响

目的 初步探讨烟酰胺对紫外线（UV）所致光老化皮肤真皮羟脯氨酸（HP）含量是否有影响。方法 利用无毛昆明种小鼠动物模型模拟慢性工期紫外线照射所致的皮肤光老化，采用UVB和UVA混合光源，经17周剂量由1MED渐增至3MED的紫外线照射背部皮肤，然后观察15周，测定真皮HP含量。分组方法：非紫外线照射组（不施加任何处理因素）；烟酰胺组（照射紫外线结束30min后，0.2mol/L烟酰胺丙酮溶液200μl涂抹于小鼠背部皮肤，每周2次）；丙酮对照组（照射紫外线30min后，90％丙酮溶液200μl涂抹小鼠背部皮肤，每周2次）；紫外线照射组（仅照射紫外线）。结果 小鼠背部皮肤HP含量烟酰胺组明显高于紫外线照射和丙酮对照组（P＜0．01）。各组腹部真皮HP含量差异均无显著性（P＞0．05）。非紫外线照射组，烟酰胺组背，腹真皮HP含量自身比较差异均无显著性，而紫外线照射组，丙酮对照组 ，腹真皮HP含量差异有显著性（P＜0．01），腹部明显高于背部。结论 皮肤涂抹烟酰胺可抵抗由皮肤光老化引起真皮HP含量降低。     

Dermabrasion

This review presents skin anatomy, dermabraders, indications for dermabrasion and microdermabrasion, and dermabrasion techniques for the face, along with potential complications. Dermabrasion is a minimally invasive technique used for skin resurfacing. Its applications include treatment of rhytids, abnormal scarring, and premalignant lesions. The risks of complications are low and include pigment changes, hypertrophic scarring, and infection. Despite the introduction of newer therapies, such as lasers and chemical peels, dermabrasion remains an effective tool for physicians to combat the effects of aging without the downtime required for surgery.     

The role of vitamin E in normal and damaged skin

The generation of free oxygen radicals is believed to play an important pathogenic role in the development of various disorders. More than other tissues, the skin is exposed to numerous environmental chemical and physical agents such as ultraviolet light causing oxidative stress. In the skin this results in several short- and long-term adverse effects such as erythema, edema, skin thickening, wrinkling, and an increased incidence of skin cancer or precursor lesions. However, accelerated cutaneous aging under the influence of ultraviolet light, usually termed photoaging, is only one of the harmful effects of continual oxygen radical production in the skin. Others include cutaneous inflammation, autoimmunological processes, keratinization disturbances, and vasculitis. Vitamin E is the major naturally occurring lipid-soluble non-enzymatic antioxidant protecting skin from the adverse effects of oxidative stress including photoaging. Its chemistry and its physiological function as a major antioxidative and anti-inflammatory agent, in particular with respect to its photoprotective, antiphotoaging properties, are described by summarizing animal studies, in vivo tests on human skin and biochemical in vitro investigations. The possible therapeutic use in different cutaneous disorders, and pharmacological and toxicological aspects are discussed. Many studies document that vitamin E occupies a central position as a highly efficient antioxidant, thereby providing possibilities to decrease the frequency and severity of pathological events in the skin. For this purpose increased efforts in developing appropriate systemic and local pharmacological preparations of vitamin E are required.