onounced, indicating that OA could increase the content material of intracellular lipid, and PCE could inhibit the lipid production induced by OA in a dose-dependent manner. In Figure 6(d), the lipids in HepG2 cells had been stained with Nile red to emit red fluorescence. Compared using the typical group without having OA induction, the model group showed stronger fluorescence intensity, as well as the fluorescence intensity progressively weakened using the enhance of PCE dose. Furthermore, we also examined the therapeutic effects of some characteristic elements of PCE on hyperlipidemia model cells, like emodin, cynaroside, polydatin, and resveratrol. In Figure 1(b), there were clear red lipid droplets in HepG2 cells induced by OA. All four monomer treatments could cut down lipid production in HepG2 cells induced by OA. All the above outcomes recommended that PCE could significantly cut down the adipogenesis of HepG2 cells induced by OA and might possess a particular preventive effect on hyperlipidemia. Among the compounds, resveratrol and polydatin possess the strongest lipid-lowering effects, suggesting that resveratrol and polydatin may be the main active ingredients for PCE to lower blood lipids. These experimental benefits confirmed the predicted benefits of network pharmacology. three.7.two. PCE Reduces OA-Induced ROS Production in HepG2 Cells. Further, the fluorescent probe DHE was employed to investigate no matter whether PCE could inhibit ROS generation beneath OA stimulation and also the OS brought on by ROS. As shown by Figure 7(a), when the cells had been treated with 0.six mM OA, the ROS developed inside the cells enhanced sharply comparedOxidative Medicine and Cellular Longevity5 4 three 2 1 0 Phospholipase C-activating G protein-coupled receptor signaling pathway Endocardial cushion morphogenesis Regulation of heart morphogenesis Epidermal growth issue receptor signaling pathway Endocardial cushion improvement Positve regulation of Calcium Channel Inhibitor medchemexpress pathway-restricted SMAD protein phosphorylation Positive regulation of epithelial to mesenchymal transition ERBB signaling pathway Mesenchyme morphogenesis Regulation of phosphatidylinositol 3-kinase CCR8 Agonist Molecular Weight activity Constructive regulation of cytosolic calcium ion concentration Urogenital technique development 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 complicated, transferring phosphorus-containing groups phosphatidylinositol 3-kinase complex Extrinsic component of membrane Membrane raft Membrane microdomain Membrane region 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 growth issue receptor signaling pathway ERBB signaling pathway Endocardial cushion development Regulation of heart morphogenesis Endocardial cushion improvement Positvie relgulation of pathway-restricted SMAD protein phosphorylation Good regulation of epithelial to mesenchymal transition Mesenchyme morphogenesis Regulation of phosphatidylinositol 3-kinase activity Transferase complicated, tran