皮肤光老化机制研究进展

光老化指皮肤由于反复光暴露引起的提前老化,其发生机制涉及细胞内信号转导通路、细胞表面细胞因子和表皮生长因子受体的活化,活性氧族是激发细胞信号转导过程中的重要介质,其结果导致基质金属蛋白酶合成增加,从而使真皮纤维结缔组织过度降解和弹性纤维变性,同时真皮胶原的合成亦减少,角质形成细胞、成纤维细胞及炎症浸润细胞等多种细胞参与光老化过程.     

皮肤光老化信号通路及激光、强脉冲光对信号通路影响的研究新进展

皮肤光老化是紫外线长期照射造成的皮肤老化,其是一个复杂的进程,涉及MAPK,TGFβ1及NF-κB等多条信号通路。激光和强脉冲光通过调控多条信号通路,促进成纤维细胞增生、胶原合成增加及细胞外基质沉积,从而导致真皮重塑,使肌肤年轻化,故在临床中广泛用于光老化防治。本文就皮肤光老化信号通路及激光、强脉冲光对多条信号通路影响机制的新进展进行综述,期望能为进一步指导临床精确治疗,开展治疗新技术,早期防治光老化提供参考依据。     

无创性检查方法在皮肤光老化的研究进展

皮肤光老化的评测方法是皮肤科研究领域中的一个关键问题。光老化指皮肤受到长期的日光照射而出现的临床、病理及功能上的改变。通常光老化是慢性紫外线损伤与自然老化叠加的结果。在表皮内,紫外线（UV）照射可诱导表皮角质形成细胞和黑素细胞突变,促使皮肤恶性肿瘤的发生;可诱导基底细胞层和毛球内的干细胞凋亡,导致表皮萎缩、伤口愈合缓慢和脱色性假瘢;而在衰老黑素细胞内发现的大量黑素合成可能是导致某些光老化皮肤永久性着色的主要原因。在真皮内,Ⅰ型胶原是成纤维细胞产生的最主要蛋白质,其含量随年龄的增加而降低［1］……     

皮肤光老化组织学改变研究进展

皮肤光老化是不断累积的日光照射所致的一个连续性过程,是指长期的日光照射(主要是紫外线)导致皮肤衰老.在组织学方面,表皮变化主要是角质形成细胞、黑素细胞、朗格汉斯细胞,真皮变化主要是弹力纤维变性和胶原减少.其机制主要涉及免疫系统、细胞因子改变、基质金属蛋白酶生成增加、活性氧簇增加及DNA损伤等.概述并探讨皮肤光老化组织学变化及其相应的发生机制.     

光老化皮肤在皮肤磨削术后的临床改善与胶原I合成相关

皮肤磨削术是光化性角化病、光化性雀斑样痣和光老化性皱纹的成功治疗方法,但对其特殊的生物学机制了解甚少。有报告,皮肤磨削术,真皮乳头出现表皮下新生胶原带或“修复带”,可能对皮肤磨削术后的临床改善起作用。推测此带是新合成的Ⅰ型胶原。本文对此进行了进一步研究,10例光老化病人(年龄48～81岁,平均59岁),临床上均有严重的面部光老化,行面部皮肤磨削术直至真皮乳头水平。临床光老化严重程度以单盲方式对皮肤磨削前基线     

皱纹与皮肤光老化

皱纹是皮肤光老化的重要特点之一,临床上以皮肤粗糙,皱褶深大、不易平复为特征。从真皮病理改变、基底膜变化和真皮变化等组织学方面综述与光老化有关的皮肤皱纹的病理学改变,阐述皮肤光老化在皮肤皱纹形成中的作用。为进一步治疗和预防光老化皱纹提供依据和思路。     

强脉冲光-光动力疗法治疗光老化的进展

皮肤光老化的机制及治疗是近些年皮肤科关注的热点,如何有效延缓或逆转光老化的进程,达到美容嫩肤的效果具有重要的应用价值。强脉冲光一光动力疗法作为一种非剥脱性光子嫩肤术,显示出广阔的应用前景。比较几种光敏剂的性状及疗效,提出如何优化治疗方案、达到满意疗效的同时降低不良反应具有临床意义。强脉冲光一光动力疗法治疗皮肤光老化的细胞和分子机制尚不十分明确,研究表明其能显著改善皮肤超微结构,可能是通过真皮成纤维细胞的细胞外信号调节激酶通路发挥作用,是否影响其他老化相关的通路,尚需进一步研究。     

果酸在皮肤科的应用

果酸是一种天然无毒的酸,可以降低角质形成细胞的黏着性,加速表皮细胞脱落与更新,同时刺激真皮胶原合成、黏多糖增加及弹力纤维的修复,对抗光老化,改善皮肤干燥,修复屏障功能,已被广泛应用于美容护肤领域。本文就果酸的历史发展、化学种类、作用机制、临床应用、不良反应进行综述。     

皮肤美容及整容

20 0 140 2 4　皮肤老化与光老化 /冯信中 (上海二医大瑞金医院皮肤科 )…∥中华医学美学美容杂志 .- 2 0 0 1,7(3) .- 16 4～ 16 6皮肤老化是一种自然过程 ,与环境和皮肤的种类有密切关系 ;而皮肤的光老化的原因主要与太阳光中的 UVA有关 ,UVB仅有 10 %～ 30 %能穿透表皮 ,UVA可协同 UVB导致真皮弹力纤维老化。黑素细胞可摄取细胞游离基因 ,防止细胞老化 ,该细胞随年龄的增加而减少。皮肤老化带来的一些生理、病理改变 ,如保护功能降低、毛发色泽的改变以及一些日光角化现象 ,部分改变是癌前期的信号。光老化可以预防 ,使用维 A酸霜 …     

染料木黄酮对预防成纤维细胞光化学损伤的影响

目的 探讨染料木黄酮在PUVA所致体外培养真皮成纤维细胞光老化模型中的保护作用。 方法　运用PUVA联合构建体外培养真皮成纤维细胞光老化模型,噻唑蓝比色法（MTT法）确定染料木黄酮最适光保护作用浓度,倒置显微镜下观察细胞形态,酶组织化学法观察细胞衰老相关-β-半乳糖苷酶（SA-β-Gal）表达,流式细胞仪检测细胞活性氧（ROS）含量,实时荧光定量PCR检测细胞基质金属蛋白酶1（MMP-1）mRNA表达等。 结果　UVA照射后24 h,正常对照组、光老化组及染料木黄酮组SA-β-Gal阳性细胞率分别为（0.67 ± 0.58）%、（96.67 ± 1.53）%、（51.67 ± 2.08）%,各组间差异有统计学意义（P ＜ 0.01）。光老化组、染料木黄酮组ROS含量分别为正常对照组的（1.88 ± 0.24）和（1.62 ± 0.02）倍（均P ＜ 0.01）。光老化组MMP-1 mRNA表达上调为正常对照组的10倍,染料木黄酮组表达量仅为正常对照组的6倍,各组间差异有统计学意义（P ＜ 0.05）。结论　染料木黄酮对PUVA所致体外培养真皮成纤维细胞光老化具有一定的保护作用。 【关键词】 染料木黄酮; PUVA疗法; 成纤维细胞; 光; 细胞衰老     

皮肤光老化发生机制的研究进展

皮肤光老化是由于紫外线的长期慢性辐射损害而造成的皮肤损伤,在临床表现、组织病理学等方面与自然老化有着不同的表现.近年国内外关于光老化发生机制方面的研究有了很大的进展,研究已经证实,激活蛋白-1和核因子-кB活化导致基质金属蛋白酶的合成、线粒体损伤、蛋白质氧化和端粒在光老化发生中的作用.理解并认识这些发生机制有助于在防治慢性紫外线辐射造成的皮肤损伤方面提出新的预防和治疗策略.     

Photoaging of human skin

Chronic sun exposure causes photoaging of human skin, a process that is characterized by clinical, histological and biochemical changes which differ from alterations in chronologically aged but sun-protected skin. Within recent years, substantial progress has been made in unraveling the underlying mechanisms of photoaging. Induction of matrix metalloproteinases as a consequence of activator protein (AP)-1 and nuclear factor (NF)-KB activation as well as mutations of mitochondrial DNA have been identified recently. This has increased our understanding of photoaging significantly and has led to new prophylactic and therapeutic strategies aimed at the prevention and repair of the detrimental effects of chronic sun-exposure on the skin.     

肥大细胞在慢性光损伤中的变化及研究进展

慢性光损伤是最常见的皮肤损害,由于长期接受紫外线照射所导致。研究表明,长期曝光部位皮肤中肥大细胞的数量较非曝光部位明显增多;肥大细胞在紫外线诱导的皮肤免疫抑制中发挥一定的作用。在慢性光损伤过程中,肥大细胞通过分泌基质金属蛋白酶和类胰蛋白酶等,参与光损伤中细胞外基质及基底膜的破坏;又通过分泌细胞因子如IL-10等,限制了小鼠皮肤慢性光损伤的病理过程。     

Protective role of adipose-derived stem cells and their soluble factors in photoaging

As individuals age, the skin undergoes changes, such as irregular pigmentation, thinning and loss of elasticity, that are due to both genetic and environmental factors. These changes may worsen, progressing to precancerous and cancerous diseases. Various medical treatments and topical cosmeceuticals have been used to treat some symptoms of photoaging, however, the results have been less than satisfactory. Mesenchymal stem cells within the stromal-vascular fraction of subcutaneous adipose tissue, adipose-derived stem cells (ADSCs), display multi-lineage developmental plasticity and secrete various growth factors that control and manage the damaged neighboring cells. Recently, the production and secretion of growth factors has been reported as an essential function of ADSCs, and diverse regenerative effects of ADSCs have been demonstrated in the skin. For example, conditioned medium from ADSCs (ADSC-CM) stimulated both collagen synthesis and migration of dermal fibroblasts, which improved the wrinkling and accelerated wound healing in animal models. ADSC-CM also inhibited melanogenesis in B16 melanoma cells, and protected dermal fibroblasts from oxidative stress induced by chemicals and UVB irradiation. Therefore, ADSCs and soluble factors show promise for the treatment of photoaging, and this review introduces recent research developments of the ADSCs and ADSC-derived secretory factors regarding this issue.     

抗皮肤光老化的研究进展

皮肤光老化逐渐被人们关注,目前针对皮肤光老化的定义以及引起皮肤不同光老化程度的最大影响因素是紫外线,提出了多种预防和治疗方法,如外用阻断紫外线照射的防晒剂、抗氧化剂和抗光老化的药物化妆品,口服含有各种维生素、微量元素的抗氧化剂和抗光老化的药物,并在平时日常生活中注意多食用些富含抗氧化成分的膳食,以及最新研究发现了一种新的抗光老化物质：来自脂肪的衍生干细胞。也可使用各种激光治疗和肉毒素或胶原蛋白等注射治疗,甚至必要时行外科手术。概述皮肤光老化的临床特点及新的常用的一些防护治疗措施及其相应的治疗原理等。     

Vitamin A antagonizes decreased cell growth and elevated collagen-degrading matrix metalloproteinases and stimulates collagen accumulation in naturally aged human skin

Damage to human skin due to ultraviolet light from the sun (photoaging) and damage occurring as a consequence of the passage of time (chronologic or natural aging) are considered to be distinct entities. Photoaging is caused in part by damage to skin connective tissue by increased elaboration of collagen-degrading matrix metalloproteinases, and by reduced collagen synthesis. As matrix metalloproteinase levels are known to rise in fibroblasts as a function of age, and as oxidant stress is believed to underlie changes associated with both photoaging and natural aging, we determined whether natural skin aging, like photoaging, gives rise to increased matrix metalloproteinases and reduced collagen synthesis. In addition, we determined whether topical vitamin A (retinol) could stimulate new collagen deposition in sun-protected aged skin, as it does in photoaged skin. Sun-protected skin samples were obtained from 72 individuals in four age groups: 18-29 y, 30-59 y, 60-79 y, and 80+ y. Histologic and cellular markers of connective tissue abnormalities were significantly elevated in the 60-79 y and 80+ y groups, compared with the two younger age groups. Increased matrix metalloproteinase levels and decreased collagen synthesis/expression were associated with this connective tissue damage. In a separate group of 53 individuals (80+ y of age), topical application of 1% vitamin A for 7 d increased fibroblast growth and collagen synthesis, and concomitantly reduced the levels of matrix-degrading matrix metalloproteinases. Our findings indicate that naturally aged, sun-protected skin and photoaged skin share important molecular features including connective tissue damage, elevated matrix metalloproteinase levels, and reduced collagen production. In addition, vitamin A treatment reduces matrix metalloproteinase expression and stimulates collagen synthesis in naturally aged, sun-protected skin, as it does in photoaged skin.     

紫外线抑制免疫系统的研究进展

由于臭氧层损耗,使地球表面的紫外线辐射量增加。紫外线不但引起皮肤晒黑、红斑、色素沉着及光老化等急慢性皮肤损伤,而且通过影响朗格汉斯细胞的抗原提呈功能、诱导调节性T细胞形成、损伤DNA、影响角质形成细胞合成与释放细胞因子、影响尿刊酸代谢、神经内分泌等途径抑制皮肤免疫系统,最终发生皮肤肿瘤。     

光老化皮肤中树突细胞及细胞因子的变化

光老化皮肤中树突细胞的数量、形态、功能及细胞因子的含量较之在自然老化皮肤中有一定的差异.这种差异导致光老化皮肤免疫能力受到抑制,甚至能够抑制伞身免疫系统,引起皮肤树突细胞数量的减少、失去特有的树突状形态以及使免疫调节性细胞因子.如白介素-10和12的含量发生一系列的变化.简要综述光老化皮肤中树突细胞及各种细胞因子的变化及其在免疫抑制过程中发挥作用的研究进展.