关键词: COX-2 HaCaT keratinocytes MMPs UVA hydroxysafflor yellow A (HSYA) oxidative stress

Mesh : Humans Quinones / pharmacology Ultraviolet Rays / adverse effects Keratinocytes / drug effects radiation effects metabolism Chalcone / pharmacology analogs & derivatives Cell Survival / drug effects radiation effects Reactive Oxygen Species / metabolism HaCaT Cells Oxidative Stress / drug effects radiation effects Cyclooxygenase 2 / metabolism genetics Matrix Metalloproteinase 9 / metabolism genetics Lipid Peroxidation / drug effects Cell Line Matrix Metalloproteinase 2 / metabolism genetics

来  源:   DOI:10.3390/ijms25147573   PDF(Pubmed)

Abstract:
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.
摘要:
评价羟基红花黄色素A(HSYA)对紫外线A(UVA)诱导的HaCaT角质形成细胞损伤的影响。HaCaT角质形成细胞经UVA照射,以及HSYA对细胞活力的影响,活性氧(ROS)的产生,脂质过氧化,和信使(m)RNA表达被测量。通过实时聚合酶链反应(RT-PCR)检测基质金属蛋白酶(MMP)-1,MMP-2,MMP-9和环氧合酶(COX)-2的mRNA表达。UVA暴露导致HaCaT角质形成细胞中细胞活力降低和ROS生成增加。HSYA有效增加UVA暴露后HaCaT角质形成细胞的活力,并保护它们免受UVA诱导的氧化应激。此外,HSYA抑制UVA诱导的HaCaT角质形成细胞的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可以充当自由基清除剂。HSYA有可能成为对抗UVA诱导的光损伤的皮肤保护成分。
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