Protective Effect of Ectoin on UVA/H2O2-Induced Oxidative Damage in Human Skin Fibroblast Cells

Abstract

Ectoin is an amino acid derivative that can create a balance between the osmotic pressure of cells and can protect enzymes, DNA proteins, and nucleic acids under extreme conditions. Ectoin has also been reported to slow skin aging. However, there are few reports on the protective effect of Ectoin on oxidative damage, especially on the regulation of PI3K/AKT-pathway-related genes at the mRNA level. UVA-induced oxidative stress injury and H2O2-induced oxidative stress injury are two common oxidative stress injury models. Skin fibroblasts produce a large number of ROS following excessive UV radiation or oxidative stimulation by H2O2, which further inhibits cell proliferation and causes cell apoptosis. In this study, UVA- and H2O2-induced oxidation models of human skin fibroblasts were established separately to investigate the protective effect of Ectoin. Further studies on the mechanisms involved, for example, the expression levels of genes associated with the PI3K/AKT signaling pathway and levels of antioxidant enzymes in cells, were determined. We found that Ectoin upregulated genes associated with the PI3K/AKT signaling pathway, including COL1A1, COL1A2, FN1, IGF2, NR4A1, and PIK3R1, but decreased intracellular ROS levels and malondialdehyde (MDA), while increasing the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). In conclusion, our results indicate that Ectoin exerts protective properties by the upregulated genes COL1A1, COL1A2, FN1, IGF2, NR4A1, and PIK3R1 and upregulating antioxidative enzyme levels.