Project description:Berberin has been shown to inhibit HepG2 cell viability. This study aims to determine the genes regulated by berberine and clarify the possible molecular mechanism underlying the action.
Project description:Berberine, an isoquinoline alkaloid isolated from many medicinal herbs such as Coptis chinensis, has a wide range of pharmacological effects including anti-cancer effects. Since xenobiotic drug-induced micoRNAs have recently emerged as key regulators in guiding their pharmacological effects and toxicity, we were interested in whether or not micoRNA expression was differentially altered by berberine treatment in HCC. Here, we used miRNA microarray to analyze microRNA expression profiles of HepG2 human hepatoma cell line after berberine chloride treatment or 0.08% DMSO as control. Comparing miRNA profiles of 40 M-BM-5M-BM--M berberine-treated HepG2 human hepatoma cell line to those of control cells sampled after 2 and 4 hours treatment. A 50 mM stock solution of Berberine chloride was prepared in DMSO. Cells were treated with 40 M-BM-5M-BM--M berberine chloride or 0.08% DMSO as control.
Project description:Berberine, an isoquinoline alkaloid isolated from many medicinal herbs such as Coptis chinensis, has a wide range of pharmacological effects. Here, we used gene expression microarray to analyze gene expression profiles of HepG2 human hepatoma cell line after berberine chloride treatment or 0.08% DMSO as control. Comparing gene expression profiles of 40 M-BM-5M-BM--M berberine-treated HepG2 human hepatoma cell line to those of control cells sampled after 4 hours treatment. A 50 mM stock solution of Berberine chloride was prepared in DMSO. Cells were treated with 40 M-BM-5M-BM--M berberine chloride or 0.08% DMSO as control.
Project description:Berberine shows protective effect against AAPH-damaged C17.2 neural stem cells. This study aims to determine the genes regulated by berberine and clarify the possible molecular mechanism underlying the action.
Project description:Berberine, an isoquinoline alkaloid isolated from many medicinal herbs such as Coptis chinensis, has a wide range of pharmacological effects including anti-cancer effects. Since xenobiotic drug-induced micoRNAs have recently emerged as key regulators in guiding their pharmacological effects and toxicity, we were interested in whether or not micoRNA expression was differentially altered by berberine treatment in HCC. Here, we used miRNA microarray to analyze microRNA expression profiles of HepG2 human hepatoma cell line after berberine chloride treatment or 0.08% DMSO as control.
Project description:Berberine, an isoquinoline alkaloid isolated from many medicinal herbs such as Coptis chinensis, has a wide range of pharmacological effects. Here, we used gene expression microarray to analyze gene expression profiles of HepG2 human hepatoma cell line after berberine chloride treatment or 0.08% DMSO as control.
Project description:Berberin has been shown to inhibit 3T3L1 preadipocytes differentiation. This study aims to determine the genes regulated by berberine and clarify the possible molecular mechanism underlying the action.
Project description:Insulin resistance (IR) is likely to induce metabolic syndrome and type 2 diabetes mellitus (T2DM). Gluconeogenesis (GNG) is a complex metabolic process that may result in glucose generation from certain non-carbohydrate substrates. Chinese herbal medicine astragalus polysaccharides and berberine have been documented to ameliorate IR, and combined use of astragalus polysaccharide (AP) and berberine (BBR) are reported to synergistically produce an even better effect. However, what change may occur in the GNG signaling pathway of IR-HepG2 cells in this synergistic effect and whether AP-BBR attenuates IR by regulating the GNG signaling pathway remain unclear. For the first time, we discovered in this study that the optimal time of IR-HepG2 cell model formation was 48 hours after insulin intervention. AP-BBR attenuated IR in HepG2 cells and the optimal concentration was 10mg. AP-BBR reduced the intracellular H2O2 content with no significant effect on apoptosis of IR-HepG2 cells. In addition, a rapid change was observed in intracellular calcium current of the IR-HepG2 cell model, and AP-BBR intervention attenuated this change markedly. The gene sequencing results showed that the GNG signaling pathway was one of the signaling pathways of AP-BBR to attenuate IR in IR-Hepg2 cells. The expression of p-FoxO1Ser256 and PEPCK protein was increased and the expression of GLUT2 protein was decreased significantly in the IR-HepG2 cell model, and both of these effects could be reversed by AP-BBR intervention. AP-BBR attenuated IR in IR-HepG2 cells, probably by regulating the GNG signaling Pathway.