Marine Biotechnology Center for Pharmaceuticals and Foods, College of Medical and Life Sciences, Silla University, Busan 46958, Korea.
Department of Food and Nutrition, College of Medical and Life Sciences, Silla University, Busan 46958, Korea.
Molecules. 2020 Mar 14;25(6):1331. doi: 10.3390/molecules25061331.
UV irradiation is one of the main causes of extrinsic skin aging. UV-mediated skin aging, also known as photoaging, causes excessive breakdown of extracellular matrix which leads skin to lose its elasticity and strength. Several phytochemicals are known to exert anti-photoaging effects via different mechanisms, partly due to their antioxidant properties. The current study has been carried out to determine the potential anti-photoaging properties of myricetin 3-O-β-d-galacto-pyranoside (M3G), a flavonol glycoside isolated from , in UVA-irradiated in vitro models; HaCaT keratinocytes and human dermal fibroblasts (HDFs). UVA-induced changes in MMP-1 and collagen production have been observed in HaCaT keratinocytes and HDFs. Further, UVA-induced activation of MAPK signaling, and pro-inflammatory cytokine production have been investigated. TGFβ/Smad pathway has also been analyzed in UVA-irradiated HDFs. Treatment with M3G reversed the UVA-induced changes in MMP-1 and collagen production both in HaCaT keratinocytes and HDFs. UVA-mediated activation of p38, ERK and JNK MAPK activation was also inhibited by M3G treatment in HaCaT keratinocytes. In HDFs, M3G was able to upregulate the TGFβ/Smad pathway activation. In addition, M3G downregulated the UVA-induced pro-inflammatory cytokines in keratinocytes and HDFs. It has been suggested that the M3G has exerted potential antiphotoaging properties in vitro, by attenuating UVA-induced changes in MMP-1 and collagen production in keratinocytes and dermal fibroblasts.
紫外线照射是导致外源性皮肤衰老的主要原因之一。紫外线介导的皮肤衰老，也称为光老化，导致细胞外基质过度分解，使皮肤失去弹性和强度。几种植物化学物质被认为通过不同的机制发挥抗光老化作用，部分原因是它们具有抗氧化特性。本研究旨在确定从 中分离得到的黄酮醇糖苷杨梅素 3-O-β-d-半乳糖吡喃糖苷（M3G）在 UVA 体外照射模型中的潜在抗光老化特性；HaCaT 角质形成细胞和人真皮成纤维细胞（HDFs）。在 HaCaT 角质形成细胞和 HDFs 中观察到 UVA 诱导的 MMP-1 和胶原蛋白产生的变化。此外，还研究了 UVA 诱导的 MAPK 信号转导和促炎细胞因子的产生。还分析了 TGFβ/Smad 通路在 UVA 照射的 HDFs 中。M3G 处理可逆转 UVA 诱导的 MMP-1 和胶原蛋白产生的变化，在 HaCaT 角质形成细胞和 HDFs 中均如此。M3G 处理还抑制了 UVA 介导的 HaCaT 角质形成细胞中 p38、ERK 和 JNK MAPK 的激活。在 HDFs 中，M3G 能够上调 TGFβ/Smad 通路的激活。此外，M3G 下调了角质形成细胞和 HDFs 中 UVA 诱导的促炎细胞因子。研究表明，M3G 通过减轻 UVA 诱导的角质形成细胞和真皮成纤维细胞中 MMP-1 和胶原蛋白产生的变化，在体外发挥了潜在的抗光老化作用。
