## 4 Discussion  
One of the main causes of skin aging is oxidative damage to the skin [38]. ROS are oxygen-containing small species, such as \({}^{1}\)O\({}_{2}\), O\({}_{3}\), OH\(\bullet\), H\({}_{2}\)O\({}_{2}\), and O\({}_{2}\bullet-\)[39]. Previous studies have shown that a large amount of ROS production can lead to oxidative stress, and oxidative damage can be caused when excessive ROS cannot be properly removed [39]. H\({}_{2}\)O\({}_{2}\) is the main ROS, and it can directly or indirectly cause cell injury and induce cell death [40,41]. In addition, ultraviolet radiation is another important source of ROS production. Long-term exposure to ultraviolet radiation will damage the structure and function of DNA and proteins and cause other macromolecular damages. Although UVB energy is greater, UVA light can penetrate deeper into the skin to cause DNA damage. Much effort has been made to fight against skin aging as focus on cosmetic beauty has increased [42]. Therefore, H\({}_{2}\)O\({}_{2}\) and UVA can cause oxidative damage by stimulating cells to produce excessive ROS. Ectoin is a natural vital substance that was developed for cosmetic applications [29]. A study conducted using an UVA stress model showed that Ectoin protects the skin from the harmful effects of UVA-induced cell damage in a number of different ways. The study showed that UVA-induced secondary messenger release, transcription factor AP-2 activation, intercellular adhesion molecule-1 expression, and mitochondrial DNA mutation could be prevented by Ectoin [26]. We hypothesized that Ectoin could reduce the ROS produced by H\({}_{2}\)O\({}_{2}\) stimulation, thus achieving the protective effect of cells. Furthermore, we evaluated the protective effects of Ectoin using both UVA-induced and H\({}_{2}\)O\({}_{2}\)-induced oxidative HSF models. Ectoin significantly increased the cell viability of the damaged cells, indicating the effect of Ectoin in promoting HSF cell proliferation. The PI3K/AKT pathway plays an important protective role against oxidative stress and resulting apoptosis [43]. PI3 Ks are members of the lipid kinase family [36] and are activated by growth factor receptors, cell adhesion molecules, and G-protein-coupled receptors [44]. The PI3K/AKT signaling pathway is involved in many biological processes, including cell proliferation, apoptosis, angiogenesis, and glucose metabolism [45,46,47]. In our study, the expression levels of COL1A1, COL1A2, COL4A5, FN1, IGF2, NR4A1, and PIK3R1 were detected using RT-qPCR. Genes, such as IGF2, NR4A1, and PIK3R1, were upregulated, accelerating the PI3K/AKT pathway and downstream genes, such as COL1A1, COL1A2, COL4A5 (not in the UVA model), and FN1. The results showed that Ectoin could regulate the PI3K/AKT pathway at the molecular level. Resveratrol, an antioxidant additive, can partially inhibit oxidative stress and induce apoptosis by activating the PI3K/AKT pathway [48]. [PERSON] et al. found that Angelica polysaccharide can promote the activation of the PI3K/AKT signaling pathway, improve cell viability, reduce cell apoptosis and ROS production, and thus reduce the level of cell oxidative damage caused by H\({}_{2}\)O\({}_{2}\) at a concentration of 300 \(\upmu\)M [49]. Furthermore, the antioxidant enzymes play an important role in the defense against oxidative damage. Apart from the enzymes (such as SOD, CAT, and GSH-Px), ROS and MDA level are usually discussed in related studies. In this study, ROS, MDA, SOD, and GSH-Px were selected to represent levels of oxidative stress in cells. The MDA content of the experimental group treated with Ectoin decreased significantly, while levels of SOD and GSH-Px showed a significant increase, proving that Ectoin protects cells from UVA and H\({}_{2}\)O\({}_{2}\) oxidative damage. Many potential functional materials play a role in accelerating the activities of antioxidant enzymes and decreasing levels of peroxide products.