tion enrichment evaluation of overlapping genes was performed. As presented in Figure five, the leading six biological processes (BP) substantially enriched by those overlapping genes have been phospholipase Cactivating G protein-coupled receptor signaling pathway, epidermal development factor receptor signaling pathway, ERBB signaling pathway, good regulation of pathway-restricted SMAD protein phosphorylation, optimistic regulation of epithelial to mesenchymal transition, and regulation of phosphatidylinositol 3-kinase activity. The top six drastically enriched cellular components (CC) integrated transferase complexes, transferring phosphorus-containing groups, membrane raft, membrane microdomain, membrane region, and phosphatidylinositol 3-kinase complicated. The top six enriched molecular functions (MF) had been growth factor activity, 1-phosphatidylinositol-3-kinase regulator activity, phosphatidylinositol 3-kinase regulator activity, transmembrane receptor protein serine/threonine kinase binding, receptor serine/threonine kinase binding, and phosphotyrosine residue binding. KEGG signaling pathway enrichment analysis demonstrated that the main enriched signaling pathways have been FOXO signaling pathway, estrogen signaling pathway, and drug metabolism-cytochrome P450. Amongst them, FOXO and estrogen signaling pathways have been most closely connected to hyperlipidemia (Figure five). 3.7. In Vitro Experiments three.7.1. PCE Reduces OA-Induced Adipogenesis in HepG2 Cells. In line with the experimental results of CCK-8, 5, 10, and 20 g/mL have been chosen because the protected dose of PCE for subsequent experiments. Meanwhile, the administration records also demonstrated no significant cytotoxicity to OAinduced HepG2 (Figure six(a)). The effect of PCE and its active compounds on OA-induced adipogenesis was measured in HepG2 cells. As shown in Figure 6(b), oil red O (ORO) staining showed that HepG2 cells inside the handle group grew almost ovoid with clear edges, and clear red lipid droplets gathering about the nucleus were evident inOxidative Medicine and Cellular LongevityVolcano plot four.35 three.48 og10 (P-value) two.61 1.74 0.87 0 -2.66-1.77-0.89 0 0.89 1.77 2.66 log2 (Foldchange)(a)27DiseaseDrug(b)(c)(d)OPRM1 ITPR1 SKP1 CYP2B6 ADRA1A BMP2 GRM1 ESR1 GNB5 PIK3R3 0 1 2(e)four 4 4 four 4 five 5 six 6 eight four five 6 7 8Figure four: Differentially expressed genes (DEGs) identified: (a) volcano plot from the DEGs; (b) overlapped genes involving DEGs and predicted targets of PCE; (c) compound-target network; (d) hub gene network; (e) the COX-1 Inhibitor Purity & Documentation result parameters from the hub gene network.the cells from the OA-treated model group, indicating that the hyperlipidemia cell model was successfully constructed. The content material of red lipid droplets in HepG2 cells showed a decreasing trend with the increase of PCE dose, and the lipid droplets became smaller and much more intensely stained. Asshown in Figure six(c), the regular group with out OA remedy had only weak green fluorescence, and the cells emitted powerful green fluorescence soon after OA c-Rel Inhibitor custom synthesis induction, indicating that the lipid content inside the cells was drastically enhanced. Though the fluorescence intensity inside the cellsTable three: Topological parameters with the compound-target network. Name ESR1 C4 MAOA C5 C7 C8 MGAM PTK2 MMP1 C1 C9 C10 C11 C2 C3 C6 C12 GNB5 PIK3R3 Degree 11 ten 8 six six 6 five five five 5 five 5 5 4 four 4 3 two 2 Average shortest path length 1.775 two.two 1.925 two.four 2.4 two.4 two.075 2.075 two.075 two.45 2.45 two.45 two.45 two.5 2.five 2.5 two.55 2.225 two.225 Betweenness centrality 0.105266 0.063913 0.050444 0.021826 0.021826 0.018167 0.
