Heliyon (Sep 2020)

Cosmeceutical potentials of Curcuma mangga Val. extract in human BJ fibroblasts against MMP1, MMP3, and MMP13

  • Dwiyati Pujimulyani,
  • Ch. Lilis Suryani,
  • Astuti Setyowati,
  • Rr. Anisa Siwianti Handayani,
  • Seila Arumwardana,
  • Wahyu Widowati,
  • Ali Maruf

Journal volume & issue
Vol. 6, no. 9
p. e04921

Abstract

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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 (Curcuma mangga Val., denoted as C. mangga). Although many pieces of evidence reveal that C. mangga 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 C. mangga 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 H2O2-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 H2O2, 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 H2O2-treated human BJ fibroblasts as confirmed by the low levels of gene expression of MPP1, MMP3, and MMP13 after treatment with CME.

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