onounced, indicating that OA could enhance the content of intracellular lipid, and PCE could Bcl-B Inhibitor drug inhibit the lipid production induced by OA within a dose-dependent manner. In Figure six(d), the lipids in HepG2 cells had been stained with Nile red to emit red fluorescence. Compared with the typical group devoid of OA induction, the model group showed stronger fluorescence intensity, plus the fluorescence intensity steadily weakened using the boost of PCE dose. Furthermore, we also examined the therapeutic effects of some characteristic components of PCE on hyperlipidemia model cells, which includes emodin, cynaroside, polydatin, and resveratrol. In Figure 1(b), there have been obvious red lipid droplets in HepG2 cells induced by OA. All four monomer therapies could reduce lipid production in HepG2 cells induced by OA. All the above outcomes suggested that PCE could considerably decrease the adipogenesis of HepG2 cells induced by OA and could have a specific preventive impact on hyperlipidemia. Among the compounds, resveratrol and polydatin have the strongest lipid-lowering effects, suggesting that resveratrol and polydatin may well be the primary active ingredients for PCE to reduced blood lipids. These experimental final results confirmed the predicted results of network pharmacology. 3.7.two. PCE Reduces OA-Induced ROS Production in HepG2 Cells. Additional, the fluorescent probe DHE was utilised to investigate no matter if PCE could inhibit ROS generation beneath OA stimulation as well as the OS IL-2 Modulator site triggered by ROS. As shown by Figure 7(a), when the cells had been treated with 0.six mM OA, the ROS produced inside the cells elevated sharply comparedOxidative Medicine and Cellular Longevity5 4 3 two 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 pathway-restricted SMAD protein phosphorylation Optimistic regulation of epithelial to mesenchymal transition ERBB signaling pathway Mesenchyme morphogenesis Regulation of phosphatidylinositol 3-kinase activity Constructive regulation of cytosolic calcium ion concentration Urogenital program 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 Unfavorable regulation of cell-cell adhesion Transferase complicated, transferring phosphorus-containing groups phosphatidylinositol 3-kinase complicated 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 aspect activity Phosphotyrosine residue binding Phospholipase C-activating G protein-coupled receptor signaling pathway Epidermal development issue receptor signaling pathway ERBB signaling pathway Endocardial cushion improvement Regulation of heart morphogenesis Endocardial cushion improvement Positvie relgulation of pathway-restricted SMAD protein phosphorylation Positive regulation of epithelial to mesenchymal transition Mesenchyme morphogenesis Regulation of phosphatidylinositol 3-kinase activity Transferase complex, tran