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.

Irradiation with ultraviolet A (UVA) plays an important role in the pathogenesis of skin photoaging since it increases oxidative stress and inflammation in the epidermis. There is an urgent need to screen, investigate, and apply the potential anti-photoaging active ingredients. Agaricus blazei Murill (ABM) polysaccharides have a wide range of promising pharmacological applications. Previous studies have confirmed their antioxidant effect, but whether it has an anti-photoaging effect is unclear. In this study, two ABM polysaccharides (AB-J and AB-K) were obtained to discuss the potential photodamage-protective capacity. The free radical scavenging abilities in vitro, the safety assessment, and their protective effects and mechanisms on UVA-induced human fibroblasts (HSFs) were evaluated. The intracellular antioxidant enzyme levels and extracellular matrix proteins, such as COL-I and ELN, were significantly accelerated, and metalloproteinases (MMP-1, and MMP-9) were decreased by AB-J and AB-K. The Keap-1-Nrf2/ARE signaling pathway was activated, thus inducing the upregulated expression of downstream genes (Ho-1 and Nqo-1). The suppression of P38 and Jnk1 by AB-J and AB-K was speculated to be the inducer of the activation of the Keap-1-Nrf2/ARE signaling pathway. Owing to the excellent exhibition of AB-J, its safety assessment and the structural characterization are discussed further.