interleukin-8 and amentoflavone

The aim of this study was to explore the mechanism by which amentoflavone (AME) improves insulin resistance in a human hepatocellular liver carcinoma cell line (HepG2).. A model of insulin resistant cells was established in HepG2 by treatment with high glucose and insulin. The glucose oxidase method was used to detect the glucose consumption in each group. To determine the mechanism by which AME improves insulin resistance in HepG2 cells, enzyme-linked immunosorbent assay (ELISA) and western blotting were used to detect the expression of phosphatidyl inositol 3-kinase (PI3K), Akt, and pAkt; the activity of the enzymes involved in glucose metabolism; and the levels of inflammatory cytokines.. Insulin resistance was successfully induced in HepG2 cells. After treatment with AME, the glucose consumption increased significantly in HepG2 cells compared with the model group (MG). The expression of PI3K, Akt, and pAkt and the activity of 6-phosphofructokinas (PFK-1), glucokinase (GCK), and pyruvate kinase (PK) increased, while the activity of glycogen synthase kinase-3 (GSK-3), phosphoenolpyruvate carboxylase kinase (PEPCK), and glucose-6-phosphatase (G-6-Pase) as well as the levels of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and C reactive protein (CRP) decreased.. The mechanism by which treatment with AME improves insulin resistance in HepG2 cells may involve the PI3K-Akt signaling pathway, the processes of glucose oxygenolysis, glycogen synthesis, gluconeogenesis and inflammatory cytokine expression.

Topics: Biflavonoids; Carcinoma, Hepatocellular; Gene Expression Regulation, Neoplastic; Glucose; Glycogen Synthase Kinase 3; Hep G2 Cells; Humans; Insulin; Insulin Resistance; Interleukin-6; Interleukin-8; Liver Neoplasms; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Signal Transduction; Tumor Necrosis Factor-alpha

This study is to observe the protection effect of amentoflavone (AMT) in Selaginella tamariscina against TNF-alpha-induced vascular inflammation injury of endothelial cells. On the basis of TNF-alpha induced human umbilical vein endothelial cell, observe the influence of AMT on endothelial active factor, the contents of SOD and MDA, the protein expression of vascular endothelial adhesion molecules and inflammatory factor; study the effect of its common related signal pathways such as NF-kappaB; research the effect of AMT against TNF-a induced human umbilical vein endothelial cell injury by means of MTT, ELISA, Western blotting and the cell immunofluorescence. The results showed that AMT could increase the content of NO and decrease the levels of VCAM-1, E-selectin, IL-6, IL-8 and ET-1; enhance the activity of SOD, reduce the content of MDA; downregulate the protein expressions of VCAM-1, E-selectin, NF-kappaBp65 and up-regulate IkappaBalpha, attenuate the NF-kappaBp65 transfer to cell nucleus. AMT has the effect of protect vascular endothelial and maybe via the signal pathway of NF-kappaB to down-regulate the inflammation factor and oxidative damage factor of downstream.

Topics: Biflavonoids; Cell Cycle; Cell Survival; E-Selectin; Endothelin-1; Human Umbilical Vein Endothelial Cells; Humans; I-kappa B Proteins; Interleukin-6; Interleukin-8; Malondialdehyde; NF-KappaB Inhibitor alpha; Nitric Oxide; Plants, Medicinal; Protective Agents; Selaginellaceae; Superoxide Dismutase; Transcription Factor RelA; Tumor Necrosis Factor-alpha; Vascular Cell Adhesion Molecule-1