Tarozzi Andrea, Marchesi Alessandra, Hrelia Silvana, Angeloni Cristina, Andrisano Vincenza, Fiori Jessica, Cantelli-Forti Giorgio, Hrelia Patrizia
International Centre for Applied Cosmetological Research, Department of Pharmacology, University of Bologna, Bologna, Italy.
Photochem Photobiol. 2005 May-Jun;81(3):623-9. doi: 10.1562/2004-06-14-RA-200.
Ultraviolet-A (UVA) radiation causes significant oxidative stress because it leads to the generation of reactive oxygen species (ROS), leading to extensive cellular damage and eventual cell death either by apoptosis or necrosis. We evaluated the protective effects of cyanidin-3-O-beta-glucopyranoside (C-3-G) against UVA-induced apoptosis and DNA fragmentation in a human keratinocyte cell line (HaCaT). Treatment of HaCaT cells with C-3-G before UVA irradiation inhibited the formation of apoptotic cells (61%) and DNA fragmentation (54%). We also investigated antioxidant properties of C-3-G in HaCaT cells against ROS formation at apoptotic doses of UVA; C-3-G inhibited hydrogen peroxide (H2O2) release (an indicator of cellular ROS formation) after UVA irradiation. Further confirmation of the potential of C-3-G to counteract UVA-induced ROS formation comes from our demonstration of its ability to enhance the resistance of HaCaT cells to the apoptotic effects of both H2O2 and the superoxide anion (O2*-), two ROS involved in UVA-oxidative stress. Furthermore, in terms of Trolox Equivalent Antioxidant Activity, C-3-G treatment led to a greater increase in antioxidant activity in the membrane-enriched fraction than in the cytosol (55% vs 19%). The protective effects against UVA-induced ROS formation can be attributed to the higher membrane levels of C-3-G incorporation. These encouraging in vitro results support further research into C-3-G (and other anthocyanins) as novel agents for skin photoprotection.
紫外线A（UVA）辐射会导致显著的氧化应激，因为它会导致活性氧（ROS）的产生，进而导致广泛的细胞损伤，并最终通过凋亡或坏死导致细胞死亡。我们评估了矢车菊素-3-O-β-吡喃葡萄糖苷（C-3-G）对人角质形成细胞系（HaCaT）中UVA诱导的凋亡和DNA片段化的保护作用。在UVA照射前用C-3-G处理HaCaT细胞可抑制凋亡细胞的形成（61%）和DNA片段化（54%）。我们还研究了C-3-G在HaCaT细胞中对UVA凋亡剂量下ROS形成的抗氧化特性；C-3-G抑制了UVA照射后过氧化氢（H2O2）的释放（细胞ROS形成的指标）。C-3-G抵消UVA诱导的ROS形成潜力的进一步证实来自于我们证明其能够增强HaCaT细胞对H2O2和超氧阴离子（O2*-）这两种参与UVA氧化应激的ROS凋亡作用的抵抗力。此外，就Trolox等效抗氧化活性而言，C-3-G处理导致富含膜的部分抗氧化活性的增加幅度大于细胞质（55%对19%）。对UVA诱导的ROS形成的保护作用可归因于C-3-G掺入的膜水平较高。这些令人鼓舞的体外研究结果支持进一步研究C-3-G（以及其他花青素）作为皮肤光保护的新型药物。
