## 2 Materials and Methods
### Antioxidant Enzymes and ROS Levels of Oxidative Stress Damaged Cells  
As shown in Figure 3A,B,D,E, the SOD and GSH-Px vitalities reduced significantly following \(\mathrm{UVA/H_{2}O_{2}}\) damage (both \(p\) < 0.05), while MDA levels increased significantly, compared with the UVA-induced or H\({}_{2}\)O\({}_{2}\)-induced models (both \(p\) < 0.05, Figure 3C,F). Both Ectoin and ascorbic acid could significantly increase the SOD and GSH-Px activities, which had decreased due to \(\mathrm{UVA/H_{2}O_{2}}\) damage (\(p\) < 0.05, Figure 3A,B,D,E). In addition, there was no significance difference between the abilities of Ectoin and ascorbic acid to  
Figure 1: The toxicity of UVA (**A**) and H\({}_{2}\)O\({}_{2}\) (**B**) to HSF cells. The results are expressed as mean \(\pm\) SD (n = 3). Different superscripts mean significant difference (uppercase for 24 h). There are six replicates in each group.  
increase SOD activity, compared with the UVA-induced model. Moreover, Ectoin exerted a stronger increasing effect (\(p<0.01\), Figure 3B) on the UVA-induced decrease in GSH-Px levels than ascorbic acid.  
In addition, Ectoin and ascorbic acid caused a significant change in reducing MDA levels, compared with the UVA-induced model. A more significant decrease in Ectoin  
Figure 3: The antioxidant activities of Ectoin on the total SOD activities (**A,D**), GSH-Px activities (**B,E**), MDA contents (**C,F**). The uppercase (**A–C**) represents the UVA-induced damaged study, while the lowercase (**D–F**) represents the H\({}_{2}\)O\({}_{2}\)-induced damaged study. Ascorbic acid (60 \(\upmu\)g/mL, 24 h) was chosen as the positive control. The model in (**A–C**) was established by UVA (22 J/cm\({}^{2}\)), and the model in (**D–F**) was established by H\({}_{2}\)O\({}_{2}\) (1000 \(\upmu\)mol\(\cdot\)L\({}^{-1}\)). Statistical significance was determined by ANOVA test. (# \(p<0.01\), and # \(p<0.05\), compared with the Control. * \(p<0.05\), and ** \(p<0.01\), compared with the Model. $p<0.05\), and $_p<0.01\(,\)_ compared with the Ascorbic acid).  
Figure 2: The toxicity of Ectoin (**A**) to HSF cells and the repair effects of Ectoin on UVA-induced (**B**) and H\({}_{2}\)O\({}_{2}\)-induced (**C**) oxidative stress damage in HSF cells. The results are expressed as mean \(\pm\) SD (n = 3). The model in (**B**) was established by UVA (22 J/cm\({}^{2}\)), and the model in (**C**) was established by H\({}_{2}\)O\({}_{2}\) (1000 \(\upmu\)mol\(\cdot\)L\({}^{-1}\)). The discussed concentrations of Ectoin are 8 and 16 \(\upmu\)g/mL. Statistical significance was determined by ANOVA test. (# \(p<0.01\), compared with the DMEM-treated control. * \(p<0.05\), and ** \(p<0.01\), compared with the Model. n.s., \(p>0.05\)).  
treatment was observed on the UVA/H\({}_{2}\)O\({}_{2}\)-induced accumulation of MDA, compared with the positive control (Figure 3F).  
UVA/H\({}_{2}\)O\({}_{2}\) treatment could induce the production of cellular ROS. The fluorescent changes represented showed the changes in ROS levels. Fluorescence intensity was observed to have increased along with the formation of ROS. After UVA/H\({}_{2}\)O\({}_{2}\) stimulation, the release of ROS in the cells of the model groups increased (Figure 4A,C). DCF fluorescence intensity is shown in Figure 4B,D. Then, a decrease in cell fluorescence intensity was observed after the damaged cells were treated with Ectoin or ascorbic acid, which indicates that Ectoin could reduce ROS levels.