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光老化。表现、预防与治疗。

Photoaging. Manifestations, prevention, and treatment.

作者信息

Kligman L H

出版信息

Dermatol Clin. 1986 Jul;4(3):517-28.

PMID:3521997
Abstract

In recent years there has been a growing awareness that many of the so-called attributes of aging skin are, instead, a reflection of environmental assault upon exposed areas of the body. Of special import are the deleterious effects of solar radiation on dermal connective tissue, leading to the visible manifestations of photoaging. Often termed "premature aging," the salient features of the process are distinctly different from those found in normal intrinsic aging. In general, chronically irradiated skin is metabolically hyperactive with epidermal hyperplasia and neoplasia, increased production of elastic fibers, GAGs, accelerated breakdown and synthesis of collagen, and enhanced inflammatory processes. In contrast, protected aged skin is usually characterized by a slow decline in many of these components. Experimental studies with animal models have confirmed the notion that the shorter, more energetic portion of the ultraviolet spectrum (UVB) is responsible for the dermal connective tissue destruction observed in photoaged skin. More recently, it has been shown that UVA and infrared radiation contribute significantly to photoaging, producing, among other changes, severe elastosis. Because the three broad wavebands are inseparably linked in terrestrial sunlight, all are of concern in the photoaging of human skin. Photoaged skin has been thought to be irreversibly damaged. However, our findings indicate that destruction and repair go on simultaneously under continued assault by actinic radiation. The balance is shifted toward repair when the radiation stress is relieved. Both epidermis and dermis are capable of moderate self-restoration when exogenous injury ceases, either by avoidance of sunlight or by the use of broad-spectrum, high-SPF sunscreens. Repair of the dermis, characterized by broad regions of new collagen deposited subepidermally, can be pharmacologically enhanced by topical application of retinoic acid. Although early protection from sunlight, before severe photodamage occurs, is most desirable, it is deemed advisable to counsel even older persons with photoaged skin to adopt protective measures, thereby allowing repair processes to occur.

摘要

近年来,人们越来越意识到,许多所谓的皮肤老化特征实际上是身体暴露部位受到环境侵害的反映。特别重要的是太阳辐射对真皮结缔组织的有害影响,导致光老化的明显表现。这个过程通常被称为“早衰”,其显著特征与正常的自然老化明显不同。一般来说,长期受照射的皮肤代谢活跃,伴有表皮增生和肿瘤形成,弹性纤维、糖胺聚糖的产生增加,胶原蛋白的分解和合成加速,炎症过程增强。相比之下,受保护的老年皮肤通常表现为这些成分中的许多缓慢下降。对动物模型的实验研究证实了这样一种观点,即紫外线光谱(UVB)中较短、能量较高的部分是导致光老化皮肤中真皮结缔组织破坏的原因。最近,研究表明UVA和红外线辐射对光老化有显著贡献,除其他变化外,还会产生严重的弹性组织变性。由于这三个宽波段在地面阳光中不可分割地联系在一起,因此它们都与人类皮肤的光老化有关。光老化皮肤一直被认为是不可逆转地受损的。然而,我们的研究结果表明,在光化辐射的持续攻击下,破坏和修复同时进行。当辐射压力减轻时,平衡会向修复方向转移。当外源性损伤停止时,无论是通过避免阳光照射还是使用广谱、高防晒系数的防晒霜,表皮和真皮都能够进行适度的自我修复。真皮的修复以表皮下沉积新胶原蛋白的广泛区域为特征,可以通过局部应用维甲酸在药理学上得到增强。虽然在严重光损伤发生之前尽早避免阳光照射是最理想的,但建议即使是患有光老化皮肤的老年人也采取保护措施,从而使修复过程得以发生。

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