Chronic and unprotect UV exposure leads to skin oxidative stress, following accumulation of damaged cellular components and downstream activation of specific signaling pathways, culminating in premature skin aging (photoaging). In this concern, polyphenols have been proposed for the prevention of skin disorders UV-generated. In the present study, we compared gallic acid (GA) and tannic acid (TA) regarding their potentials in prevent photoaging, using cell-free assays. The most promising compound was further investigated for its photoprotection abilities in UVB-irradiated L929 fibroblasts. TA was more efficient in scavenging radicals DPPH^•, superoxide anion, peroxyl, nitric oxide and peroxynitrite, and to reduce ferric ions. Although GA and TA exhibited similar inhibitory activity towards collagenase, TA was more potent in inhibit elastase. In addition, TA presented a broader UV absorption spectrum. Furthermore, TA treatment in UVB-irradiated cells attenuated redox imbalance, as observed by its ability to inhibit ROS production, NADPH oxidase activation and depletion of endogenous antioxidant defense system. Moreover, TA treatment prevented cellular photodamage and subsequently photoaging, by inhibiting lipid peroxidation, depolarization of mitochondrial transmembrane potential, DNA damage, and MMP-1 expression, a protein closely related to the structural degeneration of the dermis extracellular matrix. In conclusion, the results indicate the potential of TA in act as anti-photoaging agent, due to its potent antioxidant, anti-collagenase and anti-elastase activities, and UV-absorption effects, and its ability in prevent oxidative stress, oxidative damages and MMP-1 induction in UVB-irradiated L929 fibroblasts.

长期和不受保护的紫外线暴露会导致皮肤氧化应激，继而是受损细胞成分的积累和特定信号通路的下游激活，最终导致皮肤过早老化（光老化）。考虑到这一点，已经提出了多酚用于预防紫外线引起的皮肤疾病。在本研究中，我们使用无细胞分析法比较了没食子酸（GA）和单宁酸（TA）在预防光老化方面的潜力。进一步研究了最有前途的化合物在UVB照射的L929成纤维细胞中的光保护能力。TA清除自由基DPPH的效率更高^•，超氧阴离子，过氧化氢，一氧化氮和过氧化亚硝酸盐，并还原铁离子。尽管GA和TA对胶原酶表现出相似的抑制活性，但TA在抑制弹性蛋白酶方面更有效。此外，TA还具有更宽的紫外线吸收光谱。此外，通过UVB照射的细胞中TA的抑制ROS产生，NADPH氧化酶激活和内源性抗氧化剂防御系统耗竭的能力，可以减轻氧化还原失衡。此外，TA处理通过抑制脂质过氧化，线粒体跨膜电位去极化，DNA损伤和MMP-1表达（一种与真皮细胞外基质的结构退化密切相关的蛋白）来防止细胞的光损伤和随后的光老化。结论，