Open AccessProtective effect of 3,5‑dicaffeoyl‑epi‑quinic acid against UVB‑induced photoaging in human HaCaT keratinocytes
Author(s) -
Jung Hwan Oh,
Fatih Karadeniz,
Jung Im Lee,
Youngwan Seo,
ChangSuk Kong
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10258
Subject(s) - hacat , photoaging , oxidative stress , proinflammatory cytokine , reactive oxygen species , antioxidant , chemistry , superoxide dismutase , heme oxygenase , pharmacology , biochemistry , biology , enzyme , heme , immunology , inflammation , genetics , in vitro
Derivatives of caffeoylquinic acid (CQA) have been studied and reported as potent bioactive molecules possessing various health benefits including antioxidant and anti‑inflammatory activities. In the present study, the protective effect of 3,5‑dicaffeoyl‑epi‑quinic acid (DCEQA) isolated from Atriplex gmelinii on UVB‑induced damages was investigated in human HaCaT keratinocytes. The effect of DCEQA against UVB‑induced oxidative stress‑mediated damages was determined measuring its ability to alleviate UVB‑induced elevation of oxidative stress, proinflammatory response and antioxidant enzyme suppression through nuclear factor‑like 2 (Nrf2). Treatment with DCEQA hindered the generation of intracellular reactive oxygen species. Increased levels of proinflammatory cytokines TNF‑α, COX‑2, IL‑6 and IL‑1β following UVB exposure were suppressed by the introduction of DCEQA. Additionally, DCEQA upregulated the mRNA and protein expression of antioxidant enzymes superoxide dismutase‑1 and heme oxygenase‑1 which were inhibited under UVB irradiation. Antioxidant enzyme regulation transcription factor Nrf2 was also upregulated in the presence of DCEQA. These results suggest that DCEQA prevents photoaging via protection of keratinocytes from UVB irradiation by ameliorating the oxidative stress and pro‑inflammatory response.