onounced, indicating that OA could improve the content material of intracellular lipid, and PCE could inhibit the lipid production induced by OA within a dose-dependent manner. In Figure 6(d), the lipids in HepG2 cells were stained with Nile red to emit red fluorescence. Compared together with the regular group without having OA induction, the model group showed stronger fluorescence intensity, along with the fluorescence intensity steadily weakened with the increase of PCE dose. In addition, we also examined the therapeutic effects of some characteristic components of PCE on hyperlipidemia model cells, such as emodin, cynaroside, polydatin, and resveratrol. In Figure 1(b), there have been clear red lipid droplets in HepG2 cells induced by OA. All 4 monomer treatment options could lower lipid production in HepG2 cells induced by OA. Each of the above results suggested that PCE could significantly reduce the adipogenesis of HepG2 cells induced by OA and may possibly possess a specific preventive effect on hyperlipidemia. Among the compounds, resveratrol and polydatin have the strongest lipid-lowering effects, suggesting that resveratrol and polydatin could be the main active ingredients for PCE to reduce blood lipids. These experimental outcomes confirmed the predicted benefits of network pharmacology. 3.7.two. PCE Reduces OA-Induced ROS Production in HepG2 Cells. Additional, the fluorescent probe DHE was utilized to investigate regardless of whether PCE could inhibit ROS generation below OA stimulation and also the OS brought on by ROS. As shown by Figure 7(a), when the cells were treated with 0.six mM OA, the ROS developed within the cells enhanced sharply comparedOxidative Medicine and Cellular Longevity5 4 3 2 1 0 Phospholipase C-activating G protein-coupled receptor HDAC1 Inhibitor Storage & Stability signaling pathway Endocardial cushion morphogenesis Regulation of heart morphogenesis Epidermal growth element receptor signaling pathway Endocardial cushion development Positve regulation of pathway-restricted SMAD protein phosphorylation Good regulation of epithelial to mesenchymal transition ERBB signaling pathway Mesenchyme morphogenesis Regulation of phosphatidylinositol 3-kinase activity Optimistic regulation of cytosolic calcium ion concentration IL-5 Antagonist Species Urogenital method improvement Regulation of pathway-restricted SMAD protein phosphorylation Activation of protein kinase activity Pathway-restricted SMAD protein phosphorylation Regulation of MAP kinase activity Regulation of lipid kinase activity Branching involved in prostate gland morphogenesis Regulation of cytosolic calcium ion concentration Negative regulation of cell-cell adhesion Transferase complex, transferring phosphorus-containing groups phosphatidylinositol 3-kinase complex Extrinsic element of membrane Membrane raft Membrane microdomain Membrane area ProBMP receptor binding 1-phosphatidylinositol-3-kinase regulator activity Phosphatidylinositol 3-kinase regulator activity Transmembrane receptor protein serine/threonine kinase binding Receptor serine/threonine kinase binding Growth factor activity Phosphotyrosine residue binding Phospholipase C-activating G protein-coupled receptor signaling pathway Epidermal development element receptor signaling pathway ERBB signaling pathway Endocardial cushion development Regulation of heart morphogenesis Endocardial cushion development Positvie relgulation of pathway-restricted SMAD protein phosphorylation Constructive regulation of epithelial to mesenchymal transition Mesenchyme morphogenesis Regulation of phosphatidylinositol 3-kinase activity Transferase complicated, tran