sferring phosphorus-containing groups Extrinsic component of membrane Membrane raft CC Membrane microdomain Membrane region Phosphatidylinositol-3-kinase complex Growth aspect activity BMP receptor binding 1-phosphatidylinositol-3-kinase regulator activity Phosphatidylinositol-3-kinase regulator activity ERβ Antagonist web Transmembrane receptor protein serine/threonine kinase binding Receptor senrine/threonine kinase binding Phosphotyrosine residue binding 0.075 0.one hundred 0.125 0.150 Gene ratio Count two 3 0.175 Target genes p.adjustBP MF0.0.0.0.Biological_processCellular_ componentMolecular_ function4(a)p.adjust FoxO signaling pathway Estrogen signaling pathway Drug metabolism-cytochrome P450 TGF-beta signaling pathway Proteoglycans in cancer Human immunodeficiency virus 1 infection Relaxin signaling pathway Apelin signaling pathway Shigellosis Acute myeloid leukemia Retinol metabolism Prolactin signaling pathway JAK-STAT signaling pathway Chronic myeloid leukemia ErbB signaling pathway Phosphatidylinositol signaling program Endocrine resistance AGE-RAGE signaling pathway in diabetic complications C-type lectin receptor signaling pathway Circadian rhythm 0 1 two three 4 5 FoxO signaling pathway Estrogen signaling pathway Proteoglycans in cancer Human immunodeficiency virus 1 infection Shigellosis Drug metabolism-cytochrome P450 TGF-beta signaling pathway Relaxin signaling pathway Apelin signaling pathway JAK-STAT signaling pathway Acute myeloid leukemia Retinol metabolism Prolactin signaling pathway Chronic myeloid leukemia ErbB signaling pathway Phosphatidylinositol signaling method Endocrine resistance AGE-RAGE signaling pathway in diabetic complications C-type lectin receptor signaling pathway Circadian rhythm 0.075 Count 2 three four five 0.100 0.125 0.150 0.0.0.0.0.Gene ratio(b)Figure 5: (a) GO functional enrichment analysis; (b) KEGG signal pathway enrichment evaluation.proliferation, and apoptosis. As shown in Figure 8, the fluorescence intensity of FOXO3 in the nucleus in the model group was considerably higher than that from the standard group immediately after OA induction, indicating that the OA induction inhibited the transfer of FOXO3 to the cytoplasm, as well as the accumulation of FOXO3 inside the nucleus elevated. Even though following administration of PCE, the fluorescence intensity inside the nucleus decreased in a dose-dependent manner, as well as the relative content of FOXO3 in the cytoplasm increased, indicating that PCE could market the CCR5 Antagonist medchemexpress phosphorylation of AKT and induce the gradual transfer of FOXO3 to the cytoplasm. As shown in Figure 9, DAPI emits blue fluorescence upon binding towards the nucleus, and also the intensity of green fluorescence and red fluorescence represents the expression degree of p-AKT and AKT, respectively. Compared with all the typical group of cells, the expression of p-AKT was significantlyinhibited inside the OA-induced cells. While compared using the model group, the fluorescence intensity of p-AKT was strengthened with an escalating dose of PCE, indicating that the mechanism of PCE for stopping and treating hyperlipidemia could be related to the enhancement of AKT phosphorylation. The expression of AKT in OA-treated cells appeared to be decreased but not statistically considerable. Subsequent WB experiments confirmed the above final results, as shown in Figure 8(b). Compared with regular cells, immediately after 24 hours of OA induction, the impact of AKT phosphorylation in HepG2 cells was drastically inhibited, although no substantial modifications in the expression of AKT had been evident. However, compared with the m
