Pujimulyani Dwiyati, Suryani Ch Lilis, Setyowati Astuti, Handayani Rr Anisa Siwianti, Arumwardana Seila, Widowati Wahyu, Maruf Ali
Faculty of Agroindustry, University of Mercu Buana Yogyakarta, Yogyakarta, 55753, Indonesia.
Biomolecular and Biomedical Research Center, Aretha Medika Utama, Bandung, 40163, Indonesia.
Heliyon. 2020 Sep 16;6(9):e04921. doi: 10.1016/j.heliyon.2020.e04921. eCollection 2020 Sep.
Oxidative stress, the disrupted oxidation-reduction mechanism in our body, is caused by the excessive exposure of free radicals and the impaired antioxidant defenses that can accelerate skin aging. Antioxidants can be obtained from nature, which are available widely in therapeutic-rich plants, such as white saffron ( Val., denoted as ). Although many pieces of evidence reveal that contains an abundance of phenolic compounds and has antioxidative effects, its cosmeceutical potentials remain unclear. The present study aimed to disclose the unexplored antiaging potentials of extract (CME) in oxidative stress-induced human BJ fibroblasts with a focus on collagen protection against pro-inflammatory mediators MMP1, MMP3, and MMP13. The oxidative stress-induced cells were treated with CME and curcumin at different doses. The results showed that treatment using CME (25 μg/mL) could maintain the collagen contents up to 18.45 ± 0.68 μg/mL in HO-treated fibroblasts (only ~26.63% reduction in collagen contents), while the figure for the negative control was the lowest (12.79 μg/mL), showing a significant reduction in collagen contents by 49.13%. In addition, the gene expression of pro-inflammatory MMPs arose significantly in BJ fibroblasts after oxidative stress induction using 200 μM HO, in which the expression for MMP1, MMP3, and MMP13 increased by 7.10, 38.96, and 2.69 times, respectively. Interestingly, CME treatment (100 μg/mL) could effectively inhibit MMP1, MMP3, and MMP13 gene expression by 3.65, 34.62, and 2.02 times, respectively. In conclusion, CME showed favorable antiaging activities in HO-treated human BJ fibroblasts as confirmed by the low levels of gene expression of MPP1, MMP3, and MMP13 after treatment with CME.
氧化应激是我们体内氧化还原机制的紊乱，它是由自由基的过度暴露和抗氧化防御受损引起的，这会加速皮肤老化。抗氧化剂可以从自然界中获取，它们广泛存在于富含治疗成分的植物中，比如白番红花（Val.，表示为 ）。尽管许多证据表明 含有丰富的酚类化合物并具有抗氧化作用，但其在药妆方面的潜力仍不明确。本研究旨在揭示 提取物（CME）在氧化应激诱导的人BJ成纤维细胞中尚未被探索的抗衰老潜力，重点是胶原蛋白对促炎介质MMP1、MMP3和MMP13的保护作用。用不同剂量的CME和姜黄素处理氧化应激诱导的细胞。结果表明，使用CME（25μg/mL）处理可使经HO处理的成纤维细胞中的胶原蛋白含量维持在18.45±0.68μg/mL（胶原蛋白含量仅降低约26.63%），而阴性对照的数值最低（12.79μg/mL），胶原蛋白含量显著降低了49.13%。此外，在使用200μM HO诱导氧化应激后，BJ成纤维细胞中促炎MMPs的基因表达显著升高，其中MMP1、MMP3和MMP13的表达分别增加了7.10倍、38.96倍和2.69倍。有趣的是，CME处理（100μg/mL）可分别有效抑制MMP1、MMP3和MMP13基因表达3.65倍、34.62倍和2.02倍。总之，CME在经HO处理的人BJ成纤维细胞中显示出良好的抗衰老活性，这在CME处理后MPP1、MMP3和MMP13的低水平基因表达中得到了证实。
