Department of Nutrition and Health Sciences, Taipei Medical University, Taipei 11031, Taiwan.
Research Center of Geriatric Nutrition, College of Nutrition, Taipei Medical University, Taipei 11031, Taiwan.
Int J Mol Sci. 2024 Jul 10;25(14):7573. doi: 10.3390/ijms25147573.
To assess the effects of hydroxysafflor yellow A (HSYA) on ultraviolet A (UVA)-induced damage in HaCaT keratinocytes. HaCaT keratinocytes were UVA-irradiated, and the effects of HSYA on cell viability, reactive oxygen species (ROS) generation, lipid peroxidation, and messenger (m)RNA expression were measured. mRNA expressions of matrix metalloproteinase (MMP)-1, MMP-2, MMP-9, and cyclooxygenase (COX)-2 were determined by a real-time polymerase chain reaction (RT-PCR). UVA exposure led to a decrease in cell viability and an increase in ROS generation in HaCaT keratinocytes. HSYA effectively increased the viability of HaCaT keratinocytes after UVA exposure and protected them from UVA-induced oxidative stress. Moreover, HSYA inhibited expressions of MMP-1, MMP-2, MMP-9, and COX-2 by HaCaT keratinocytes with UVA-induced photodamage. Our results suggest that HSYA can act as a free radical scavenger when keratinocytes are photodamaged. HSYA has the potential to be a skin-protective ingredient against UVA-induced photodamage.
评估羟基红花黄色素 A(HSYA)对 UVA 诱导的 HaCaT 角质形成细胞损伤的影响。
用 UVA 照射 HaCaT 角质形成细胞,检测 HSYA 对细胞活力、活性氧(ROS)生成、脂质过氧化和信使(m)RNA 表达的影响。采用实时聚合酶链反应(RT-PCR)检测基质金属蛋白酶(MMP)-1、MMP-2、MMP-9 和环氧化酶(COX)-2 的 mRNA 表达。
UVA 照射导致 HaCaT 角质形成细胞活力下降,ROS 生成增加。HSYA 可有效提高 UVA 照射后 HaCaT 角质形成细胞的活力,并保护其免受 UVA 诱导的氧化应激。此外,HSYA 抑制 UVA 诱导光损伤的 HaCaT 角质形成细胞中 MMP-1、MMP-2、MMP-9 和 COX-2 的表达。
我们的结果表明,当角质形成细胞受到光损伤时,HSYA 可以作为自由基清除剂。HSYA 有潜力成为一种皮肤保护成分,可预防 UVA 诱导的光损伤。