Department of Nursing, National Taichung University of Science and Technology, Taichung 40640, Taiwan.
Division of Dietetics and Nutrition, Taichung Tzu Chi Hospital, Taichung 40600, Taiwan.
Biochem J. 2019 May 21;476(10):1387-1400. doi: 10.1042/BCJ20180974.
Ultraviolet-B exposure causes an inflammatory response, photoaged skin, and degradation of extracellular matrix proteins including collagen and elastin. The regulation of these genes was suggested as an important mechanism to attenuate skin aging. Glycolic acid (GA) is commonly present in fruits and recently used to treat dermatological diseases. We reported that GA slows down cell inflammation and aging caused by UVB. Little is known about GA retarding the skin premature senescence or how to impede these events. To investigate the potential of GA to regulate the expression of MMPs and collagen, GA was topically applied onto human keratinocytes and the C57BL/6J mice dorsal skin. In the present study, we demonstrated that GA reduced UVB-induced type-I procollagen expression and secretory collagen levels. GA reverted and dose-dependently increased the level of aquaporin-3 (AQP3), the expression of which was down-regulated by UVB. The UV-induced MMP-9 level and activity were reduced by GA pre-treatment. Concomitantly, GA reverted mitogen-activated protein kinase (MMP-9) activation and inhibited the extracellular signal-regulated kinase activation (p38, pERK) triggered by UVB. The animal model also presented that GA attenuated the wrinkles caused by UVB on the mouse dorsal skin. Finally, GA triggers the transient receptor potential vanilloid-1 (TRPV-1) channel to initiate the anti-photoaging mechanism in keratinocytes. These findings clearly indicated that the mechanisms of GA promote skin protection against UVB-induced photoaging and wrinkle formation. GA might be an important reagent and more widely used to prevent UVB-induced skin aging.
紫外线-B 暴露会引起炎症反应、光老化皮肤和细胞外基质蛋白（包括胶原蛋白和弹性蛋白）的降解。这些基因的调节被认为是减轻皮肤衰老的重要机制。甘醇酸（GA）通常存在于水果中，最近用于治疗皮肤病。我们报道 GA 可减缓 UVB 引起的细胞炎症和衰老。目前对于 GA 如何延缓皮肤过早衰老或阻止这些事件知之甚少。为了研究 GA 调节 MMP 和胶原蛋白表达的潜力，我们将 GA 局部应用于人角质形成细胞和 C57BL/6J 小鼠背部皮肤。在本研究中，我们证明 GA 减少了 UVB 诱导的 I 型原胶原蛋白表达和分泌型胶原蛋白水平。GA 逆转并呈剂量依赖性增加水通道蛋白-3（AQP3）的水平，AQP3 的表达被 UVB 下调。GA 预处理可降低 UV 诱导的 MMP-9 水平和活性。同时，GA 逆转了由 UVB 触发的丝裂原活化蛋白激酶（MMP-9）的激活，并抑制了细胞外信号调节激酶的激活（p38、pERK）。动物模型也表明，GA 减轻了 UVB 对小鼠背部皮肤引起的皱纹。最后，GA 触发瞬时受体电位香草醛-1（TRPV-1）通道，在角质形成细胞中启动抗光老化机制。这些发现清楚地表明，GA 的作用机制促进了皮肤对 UVB 诱导的光老化和皱纹形成的保护。GA 可能是一种重要的试剂，并将更广泛地用于预防 UVB 诱导的皮肤衰老。
