Ultraviolet (UV) radiation is a major factor that causes wrinkle formation by affecting the collagen level in the skin. Here, we show that a short peptide (A8) derived from the repair domain of the ribosomal protein S3 (rpS3) reduces UV irradiation-induced increase in matrix metalloproteinase-1 (MMP-1) and prevents collagen degradation by reducing the activation of the mitogen-activated protein kinase (MAPK) signaling proteins (extracellular signal-regulated kinase [ERK], p38, and c-Jun N-terminal kinases [JNK]) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in cells. Furthermore, A8 also prevents the increase in the levels of inflammatory modulators such as tumor necrosis factor-alpha (TNF-α) or interleukin-6 (IL-6) in UV-irradiated cells. Collectively, our study suggests that the A8 peptide, derived from yeast or human, has anti-photoaging potential as it prevents UV-induced wrinkle formation.

紫外线（UV）辐射是通过影响皮肤中胶原蛋白水平导致皱纹形成的主要因素。在这里，我们显示了源自核糖体蛋白S3（rpS3）修复域的短肽（A8）减少了紫外线辐射诱导的基质金属蛋白酶1（MMP-1）的增加，并通过减少胶原蛋白的活化来防止胶原降解丝裂原激活蛋白激酶（MAPK）信号蛋白（细胞外信号调节激酶[ERK]，p38和c-Jun N端激酶[JNK]）和核因子kappa轻链增强子（NF -κB）。此外，A8还可以防止紫外线照射的细胞中炎症调节剂，例如肿瘤坏死因子-α（TNF-α）或白介素-6（IL-6）的水平增加。总体而言，我们的研究表明A8肽，