## Results and Discussion
### Lipid Peroxidation Inhibition Assay
#### 3.6.1 Cytotoxicity of MMP-4, MMP-7 and MMP-12 on HepG2 Cells  
Cytotoxic effects of three isolated peptides (MMP-4, MMP-7, and MMP-12) at the concentrations of 100.0 uM were determined in HepG2 cells by the MTT assay. As shown in Figure 9, MMP-4, MMP-7, and MMP-12 exhibited no significant cytotoxic effects on HepG2 cells compared to the blank control (no peptide treatment) at the tested concentrations for 24 h treatment (\(p<0.05\)). The result indicated that three isolated peptides (MMP-4, MMP-7, and MMP-12) from protein hydrolysate of monkfish muscle could serve as the candidate molecules for antioxidant food and drugs.  
Figure 8: Lipid peroxidation inhibition assays of three isolated peptides (MMP-4, MMP-7, and MMP-12) from protein hydrolysate of monkfish (_L. litulon_) muscle. The data are presented as the mean \(\pm\) SD (\(n=3\)). \({}^{\alpha-d}\) Values with the same letters indicate no significant difference of different samples at the same concentrations (\(p>0.05\)).  
Figure 9: Cytotoxicity of three isolated peptides (MMP-4, MMP-7, and MMP-12) from protein hydrolysate of monkfish (_L. litulon_) muscle on HepG2 cells at the concentration of 100.0 uM. The data are presented as the mean \(\pm\) SD (\(n=3\)).  
6.2 Protection of MMP-4, MMP-7, and MMP-12 on H\({}_{2}\)O\({}_{2}\)-induced Oxidative Damage HepG2 Cells  
Oxidative stress caused by ROS is responsible for a wide variety of cellular damage and is the most validated mechanism of secondary injury. Following oxidative stress, the overproduction of ROS and subsequently the depletion of antioxidants results in the total breakdown of the endogenous antioxidant defense mechanisms, culminates in failure to protect cells from damage induced by oxidative stress, and finally leads to significantly reduced cell viability which we try to protect with antioxidant peptides. In the present study, we showed that H\({}_{2}\)O\({}_{2}\) could damage HepG2 cells and caused cells significantly cytotoxic effects. In our previous report, H\({}_{2}\)O\({}_{2}\) at the concentration of 300 \(\upmu\)M is used to establish the oxidative stress model of HepG2 cells in the assay [2], and the cell viability reached 48.85 \(\pm\) 1.68% of control group for induced 24 h. Using the oxidative stress model of HepG2 cells, the cytoprotective effects of MMP-4, MMP-7, and MMP-12 were evaluated through measured the cell viability, ROS content, activities of antioxidant enzymes and levels of MDA.  
Figure 10 showed the influences of three isolated peptides (MMP-4, MMP-7, and MMP-12) on H\({}_{2}\)O\({}_{2}\)-induced oxidative damage HepG2 cells, and the cell viability of three isolated peptides (MMP-4, MMP-7, and MMP-12) treated groups was gradually increased in a concentration-dependent manner compared with the model group. Moreover, the MMP-12 treated group increased the HepG2 cell viability from 48.85% \(\pm\) 1.68% to 63.28% \(\pm\) 2.06%, 79.35% \(\pm\) 2.85%, and 88.65% \(\pm\) 3.42% at the concentrations of 10.0, 50.0, and 100.0 \(\upmu\)M, respectively, which were significantly higher than that of the model group (\(p<0.01\)). The finding suggested that MMP-4, MMP-7, and MMP-12 could strongly protect H\({}_{2}\)O\({}_{2}\)-induced oxidative damage HepG2 cells, especially at the high concentrations.