皮肤光老化机制研究进展

长期紫外线辐射将导致皮肤胶原纤维减少和异常弹性纤维沉积而出现皮肤光老化。近年来大量研究表明紫外线作用于人体皮肤后通过产生的活性氧、细胞表面的生长因子受体、细胞因子受体及许多酶的级联，激活转录因子激活蛋白，使基质金属蛋白酶高表达而降解细胞外基质，最终导致皮肤光老化。     

神经肽在紫外线辐射诱导皮肤光损伤性疾病中的作用

神经肽是一类小分子肽,属于细胞外信使家族,作为维系皮肤与神经-免疫-内分泌网络系统的重要信号分子,神经肽在维持皮肤内环境稳态和多种病理生理过程中起到重要的作用。近年来研究发现,当皮肤受到紫外线辐射后,中枢神经细胞、外周感觉神经纤维和皮肤细胞可分泌多种神经肽,参与调控细胞凋亡、炎症反应、黑素生成、免疫抑制、细胞外基质降解等多种急慢性皮肤光损伤发病过程。本文综述常见神经肽在皮肤光损伤性疾病中的主要作用,以期为其防治提供新的思路和分子靶点。     

光老化皮肤的预防,减慢和康复

光老化皮肤表现为发黄、革样、松垂和起皱,其下结缔组织出现损伤以及发生各种良性、癌前期或恶性肿瘤。组织学改变在青年人皮肤弹性组织的纤维是纤细、分枝的、并有垂直纤维分枝上达表皮真皮交界处。老年非暴露的皮肤,弹力     

皮肤光老化和抗氧化剂研究进展

皮肤光老化是指皮肤长期受紫外线(ultraviolet,UV)辐射引起的皮肤老化。紫外线可通过诱导活性氧和脂质过氧化物丙二醛生成,诱导金属蛋白酶类表达等途径诱发皮肤光老化。针对光老化的发病机制采用各种天然或合成抗氧化剂能够有效的预防和缓解皮肤光损伤,本文对皮肤光老化机制及治疗研究进展进行综述。     

皮肤光老化机制研究进展

长期紫外线辐射将导致皮肤胶原纤维减少和异常弹性纤维沉积而出现皮肤光老化。近年来大量研究表明紫外线作用于人体皮肤后通过产生的活性氧、细胞表面的生长因子受体、细胞因子受体及许多酶的级联 ,激活转录因子激活蛋白 ,使基质金属蛋白酶高表达而降解细胞外基质 ,最终导致皮肤光老化     

皮肤光老化治疗研究进展

预防和治疗皮肤光老化是当前研究的热点,各种抗光老化药物、化学剥脱剂、物理治疗、注射填充等方法可改善皮肤光老化症状。本文对皮肤光老化各种治疗方法的最新研究进展进行综述,以期为皮肤光老化治疗的相关研究提供一些参考。     

中波紫外线与皮肤恶性肿瘤发生机制的研究进展

皮肤癌是最常见的人类恶性肿瘤之一，而中波紫外线是诱发皮肤肿瘤的主要因素。机体细胞可通过多种途径修复紫外线引起的光损伤。某些关键基因如p53等的突变在肿瘤发生发展过程中起重要作用。     

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。     

皮肤光损伤模型的研究进展北大核心CSCD

皮肤是保护人体诸多组织、器官免受物理、化学、微生物等侵袭的天然屏障,其作为人体的最外层,直接暴露于外界环境之下,尤其是紫外线的照射会使皮肤出现一系列的光损伤,如红斑、免疫抑制、光老化、各种皮肤良恶性肿瘤等。为此成功建立皮肤光损伤的各种模型,对研究光损伤的机制,制定一系列治疗及防护措施具有重要的意义。     

紫外线致皮肤光损伤皮肤癌的机制

波长范围在280nm～320nm的中波紫外线（UVB）在光损伤皮肤癌的发展中占有重要的作用。它主要被表皮吸收,尤其表现为影响机体的免疫系统、凋亡分子等,从而诱发皮肤癌。     

Effects of temperature on ultraviolet-induced erythema of human skin

Summary Convective cooling of human skin to 20°C or less for 1 h immediately after ultraviolet-B irradiation (UV-B, 290–320 nm) results in a significant increase in erythemal threshold when erythema was observed at 4–6 h postirradiation. Cooling the skin immediately before UV-B irradiation showed no consistent influence on the erythema response. In neither case was an effect of cooling on erythemal threshold apparent when erythema was evaluated at 24 h postirradiation. These effects may be due to alterations in the diffusion kinetics of chemical mediators of inflammation, modification of vascular responsiveness, or reflect changes in temperature-dependent cellular repair or expression of UV-induced damage.This work was supported by the Wellman Laboratories     

紫外线诱导的脂质过氧化机制与相关皮肤病的研究进展

紫外线可干扰细胞的信号传导过程,诱导细胞产生过量的活性氧.脂质是生物膜的主要成分,也是活性氧的主要攻击靶点.活性氧与多不饱和脂肪酸为主的脂质发生脂质过氧化反应,在中高水平脂质过氧化作用下,细胞发生凋亡和坏死细胞的程序性死亡,最终导致细胞损伤,促进多种病理状态的发展和加速老化过程.脂质过氧化作用产生丙二醛、4羟基壬烯醛和丙烯醛等高亲电子活性的醛,这些醛类可对磷脂、蛋白质和DNA造成不可逆的修饰和损伤.脂质过氧化作用与许多皮肤病相关,对脂质过氧化作用的进一步研究可能会为皮肤病的预防与治疗提供新方法.     

Characterization of ultraviolet radiation-induced damage to keratinocytes in a skin equivalent in vitro

The human skin equivalent (HSE) provides a convenient model for studying the dermatological effects of exposure to ultraviolet (UV) radiation. HSEs, constructed by overlaying a collagen-fibroblast matrix with epidermal cells, were maintained submerged for 1 week after the addition of epidermal cells and then raised to the air-liquid interface for an additional 3 weeks. HSEs were exposed to sublethal doses of UV radiation ranging from 0 to 500 J/m², incubated up to 48 h in medium containing ³H-thymidine and fixed for ultrastructural and autoradiographic analysis. Exposure to radiation doses greater than 50 J/m² led to vacuolation of the cornified envelopes and enlargement of intercellular spaces. These doses also led to the formation of dense cytoplasmic bodies, and separation and vesiculation of the nuclear envelope in the basal cells. DNA synthesis in the basal cells was analyzed autoradiographically. Maximal numbers of labeled basal cells were observed 24 h after exposure to UV radiation at 50 J/m². Although the proportions of labeled cells varied among different epidermal donors, the maximal responses and time-course of ³H-thymidine incorporation remained consistent, supporting the usefulness of the HSE in studying the effects of UV irradiation on human skin.     

Toll样受体与紫外线致皮肤光损伤及皮肤肿瘤

紫外线辐射可导致免疫抑制、DNA损伤及皮肤肿瘤的发生.Toll样受体是重要的模式识别受体,在机体天然免疫和获得性免疫中均起重要作用.Toll样受体在皮肤角质形成细胞、朗格汉斯细胞、树突细胞、肥大细胞、成纤维细胞、黑素细胞中都有表达.激活Toll样受体相关信号通路可使与免疫应答相关的细胞因子、趋化因子、共刺激分子及黏附分子的表达增加.越来越多的研究表明,Toll样受体与紫外线辐射后细胞应答相关,以Toll样受体为靶标预防和治疗皮肤癌已愈来愈受到关注.     

Reliability and validity of a bioimpedance measurement device in the assessment of UVR damage to the skin

Ultraviolet radiation (UVR) is the primary cause of skin cancers. However, it is difficult to evaluate the amount of UVR absorbed into the skin retrospectively. Therefore, objective and non-invasive quantitative method would be valuable for epidemiological UVR exposure assessment. Photodamage reduces the amount of bound water in the skin, and thus, measuring the skin’s dielectric constant can provide an opportunity for assessing the cumulative UVR exposure. The purpose of the study was to assess the reliability and validity of the bioimpedance device, Moisture Meter-D. The measurements were performed on 100 subjects at three separate measurement times. A questionnaire was used to obtain information on the host factors and on the past UVR exposure. The biological samples, to determine the elastin proportion of the dermis, were collected. Some long-term as well as seasonal variations in the dielectric constants were detected. Also, a weak relationship between the dielectric constant and the UVR exposure indicators and host factors was observed. The MoistureMeter-D appears not to measure structural alterations in the skin caused by photodamage, and thus it is not a valid instrument for the assessment of photodamage, i.e., past UVR exposure.     

与紫外线致皮肤损伤相关的部分信号通路研究进展

紫外线照射可使皮肤损伤,导致皮肤光老化或皮肤肿瘤.多个信号通路如Nrf2-Keap1-ARE、核因子κB、丝裂原活化蛋白激酶(MAPK)、磷脂酰肌醇-3激酶-丝氨酸/苏氨酸激酶-西罗莫司靶蛋白(PI3K-AKt-mTOR)信号通路等参与皮肤光老化和(或)皮肤肿瘤的发病.Nrf2信号通路在氧化应激状态下开启,有维持氧化还原平衡和参与细胞新陈代谢等作用.核因子κB信号通路的激活引起基质金属蛋白酶等水平上调,与皮肤老化和非黑素性皮肤癌有关.MAPK信号通路参与皮肤老化和皮肤肿瘤的进展.PI3K-AKt-mTOR信号通路主要与皮肤肿瘤相关.紫外线照射可诱导上述通路的活化,参与皮肤光老化或皮肤肿瘤的发生发展.对上述通路的进一步研究有望为抵御皮肤的光老化和皮肤肿瘤提供新的方法.     

维族和汉族女性对紫外线危害的认知水平和皮肤防护现状调查

目的了解乌鲁木齐地区女性对紫外线危害的认知水平和自我皮肤防护的现状,使皮肤科医护人员更有针对性地进行个体化健康教育。方法随机抽取新疆维吾尔自治区人民医院皮肤科门诊维吾尔族和汉族女性就诊者494例进行问卷调查,采用SPSS17．0软件进行统计分析。结果知道紫外线会致光老化者占61．97％,知道防晒系数（SPF）和UVA防护等级（PA）含意的分别占46．96％（250／494）和17．21％（85／494）,认为日光弱的冬天和室内需要防晒的分别占50．69％和30．56％,汉族女性比维吾尔族女性该方面知晓率高（P〈0．01）;13岁以后开始有护肤意识的占6％,维吾尔族在13～15岁开始的占9．03％,汉族占4．08％;维吾尔族中有87．74%的女性经常使用天然物品护肤,有使用护肤品习惯的占58．0％,比汉族女性（分别占44．24％和48．37％）人数更多;维吾尔族女性不熬夜者占22．58％,汉族女性为55．21％;维吾尔族女性经常在室外活动的占6．45％,汉族女性为9．73％。结论494例受检者对紫外线的危害认知水平低,自我皮肤防护意识弱,且存在错误认知,需要加强并纠正该地区人群的皮肤防晒护肤知识宣传和自我护肤的健康教育。     

Linoleic acid and α-linolenic acid lightens ultraviolet-induced hyperpigmentation of the skin

Abstract This study was conducted to evaluate the effects of unsaturated fatty acids on ultraviolet-induced hyperpigmentation of the skin. An efficient lightening effect was observed following topical application of linoleic acid or α-linolenic acid to UV-stimulated hyperpigmented dorsal skin of brownish guinea pigs. The number of melanocytes in the treated skin was similar to the number in the skin of the pigmented control, indicating that the pigment-lightening effect was not due to depletion of melanocytes. In vitro experiments using cultured murine melanoma cells showed that melanin production was inhibited most effectively by α-linolenic acid, followed by linoleic acid and then by oleic acid. Furthermore, the turnover of the stratum corneum, which plays an important role in the removal of melanin pigment from the epidermis, was accelerated by linoleic acid and by α-linolenic acid. Taken together, the results suggest that the pigment-lightening effects of linoleic acid and α-linolenic acid are, at least in part, due to suppression of melanin production by active melanocytes, and to enhanced desquamation of melanin pigment from the epidermis. Received: 8 October 1997     

人工皮肤在紫外线对皮肤作用中的研究进展

人工皮肤作为人体皮肤形态及功能的类似物,成为研究紫外线对人体皮肤作用的新型体外模型.近5年来,国内外在光生物学领域主要用其研究皮肤光损伤的形态学、分子机制及开发防护及修复光损伤制剂.同时结构更完善的皮肤模型在该研究领域的引进,为组织工程化皮肤在紫外线皮肤损伤的基础及临床研究提供新思路.