## 3 Results and Discussion
### Effects of VIAPW (M7) and IRWWW (M10) on Lowering Intracellular TG and TC Contents
In addition, AMPK activation can increase the expression of proteins associated with FA oxidation, including carnitine palmitosyltransferase I (CPT-1), PPARs, and acyl-CoA oxidase 1 (ACOX-1) [34]. Effects of VIAPW (M7) and IRWWW (M10) on the expression levels of genes drawn into lipid synthesis (SREBP-1c, SREBP-2, FAS, ACC, and HMGR) and oxidation (PPAR\(\alpha\), ACOX-1, and CPT-1) in HepG2 cells were investigated, and the data were analyzed using the qRT-PCR method (Figure 5). In comparison with the OA model group, VIAPW (M7) could extremely significantly decrease the expression levels of genes of SREBP-1c (\(p<0.001\)), very significantly reduce the expression levels of genes of ACC and FAS (\(p<0.01\)), and significantly decrease the expression levels of genes of SREBP-2 and HMGR (\(p<0.05\)). In addition, Figure 6 indicated that VIAPW (M7) could significantly increase the expression levels of genes of PPAR\(\alpha\), ACOX-1, and CPT-1 (\(p<0.05\)). Figure 4: Effects of VIAPW (M7) and IRWWW (M10) from miniy croaker (_M. miniy_) muscle on the intracellular contents of total triglycerides (TG) (**A**) and cholesterol (TC) (**B**) in HepG2 cells at the concentrations of 10, 50, and 100 \(\upmu\)m. Simvastatin (SV) and FMPLH (M5) were used as the positive control and negative control, respectively. Means \(\pm\) SD (n = 3) are used to express the experiment data. \(\mathbf{{}^{\#}}\mathbf{{}^{\#}}\mathbf{{}^{\#}}\mathbf{{}^{\#}}\mathbf{{}^{\#}}\mathbf{{}^{\#}}\mathbf{{}^ {\#}}\mathbf{{}^{\#}}\mathbf{{}^{\#}}\mathbf{{}^  
The effect of IRWWW (M10) on the expression levels of genes related to the lipid metabolism showed a similar tendency with VIAPW (M7), but the expression levels of genes were slightly different from those of VIAPW (M7). Compared with the OA model group, IRWWW (M10) could extremely significantly down-regulate the expression level of SREBP-1c gene (\(p<0.001\)), very significantly down-regulate the expression levels of SREBP-2 genes (\(p<0.01\)), and significantly down-regulate the expression levels of genes of ACC, FAS, and HMGR (\(p<0.05\)). Moreover, IRWWW (M10) extremely significantly up-regulated the expression level of gene of CPT-1 (\(p<0.001\)) and very significantly up-regulated the expression levels of genes of PPAR\(\alpha\) and ACOX-1 (\(p<0.01\)). Lipid accumulation in hepatic cells could be induced through increasing de novo lipogenesis and lipid intake and reducing lipid \(\beta\)-oxidation. SREBP-1c and SREBP-2 are the preponderant isoforms and control the levels of ACC and HMGR in hepatic cells, which were the first enzymes recognized as downstream targets for AMPK and key enzymes in FA and TC synthesis [35]. SREBP-1c is a critical transcription factor for increasing the expression levels of lipogenesis genes and plays a significant part in the pathogenesis of hepatic steatosis [36,37]. SREBP-1c can up-regulate the expression level of lipogenic enzymes of ACC, which is responsible for the biosynthesis of malonyl-CoA as the rate-controlling enzyme. Malonyl-CoA is an essential precursor in the synthesis of FA and increases FAS. In addition, malonyl-CoA is a powerful suppressor of mitochondrial lipid oxidation through regulating the rate-limiting enzyme of CPT-1 in FA oxidation, whereas SREBP-2 was generally regarded to be involved in TC synthesis by regulating the gene expression level of HMGR, which limits the biosynthesis of TC and catalyzes the conversion of HMG-CoA into mevalonate. Down-regulating the expression level of the gene of HMGR can lead to the rapidly reducing cholesterol biosynthesis [35]. As a nuclear receptor, PPAR\(\alpha\) highly expresses in liver and plays a crucial role in the regulation of lipid metabolism [26]. Activation of PPAR\(\alpha\) can increase the expressions levels of genes drawn  
Figure 5: Effects of VIAPW (M7) and IRWWW (M10) from miuuy croaker (_M. miuuy_) muscle at a concentration of 100 \(\upmu\)m on the expression levels of genes involved in lipid synthesis ( SREBP-1c, SREBP-2, FAS, ACC, and HMGR) in HepG2 cells.