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Repair Activity of Skin Barrier by Chitin-Nanofibrils Complexes

机译:几丁质-纳米纤维复合物对皮肤屏障的修复活性

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Stratum Corneum (SC) lipids and comeodesmosomes involved in cor-neocytes and lamellar packing (1-3), and filaggrin production, responsible of the Normal Moisturizing Factors (NMF) release (4-7), are considered key components of the skin barrier together with the enzymatic antioxidant system (8). SC is composed, in fact, of nucleated keratin-rich corneocytes embedded in a extracellular lipid matrix organized into membrane-like bilayers interconnected by comeodesmosomes (9). Both corneocytes and lipid lamellae, as main component of skin barrier, are responsible for the water retention and diffusion through the skin preventing excess transepidermal water loss (TEWL), while degradation of comeodesmosomes is the key event of the regular shedding and renewing of the SC barrier (10,11). The hallmark of this barrier formation and function lies, in fact, in the intricate balance of epidermal cell differentiation and desquamation events. Nevertheless, while this orchestrated interplay of events can be influenced and perturbed by environmental stressors and ageing, too much damage can enhance epidermal hyperplasia and inflammation (12-14). As a consequence of defects in skin barrier function, mild to severe xerosis appear, which can lead to the penetration of irritants and allergens resulting in immunological and inflammatory processes (15). Atopic Dermatitis (AD) is, for example, a severe xerotic skin disease characterized by a disruption of epidermal barrier function that, increasing the reactivity to common environmental allergens, leads to an allergic-type inflammatory reaction (15-17). According to previous studies (18-20) the disruption of this barrier affecting premature aging also, should be repaired by the use of some antioxidant and immunomodulant compounds complexed with chitin nanofib-rils (CN), capable to improve its functionality. The vehicle used results, naturally, of fundamental importance.
机译:角质层(SC)脂质和角质形成小体与皮质细胞和层状堆积有关(1-3)以及丝蛋白生成与正常保湿因子(NMF)释放有关(4-7),被认为是皮肤屏障的关键成分以及酶促抗氧化剂系统(8)。实际上,SC由嵌入细胞外脂质基质中的有核的富含角蛋白的角质细胞组成,组织成膜状双层,并由粉刺体相互连接(9)。角质细胞和脂质薄片都是皮肤屏障的主要成分,它们负责水的保留和在皮肤中的扩散,防止过多的表皮水分流失(TEWL),而粉刺小体的降解是SC定期脱落和更新的关键事件。障碍(10,11)。实际上,这种屏障形成和功能的标志在于表皮细胞分化和脱皮事件的复杂平衡。然而,尽管事件之间的这种精心安排的相互作用会受到环境压力和衰老的影响和干扰,但过多的损害会加剧表皮增生和炎症(12-14)。由于皮肤屏障功能的缺陷,出现了轻度至重度的干燥症,可导致刺激物和过敏原的渗透,从而导致免疫和炎性过程(15)。特应性皮炎(AD)是一种严重的皮肤干燥性皮肤病,其特征是表皮屏障功能受到破坏,从而增加了对常见环境变应原的反应性,导致了变应性炎症反应(15-17)。根据先前的研究(18-20),也应通过使用一些能够改善其功能的复合壳多糖纳米纤维(CN)的抗氧化剂和免疫调节化合物来修复这种影响早衰的屏障。车辆使用的结果自然很重要。

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