u-0126 has been researched along with geniposide* in 2 studies
2 other study(ies) available for u-0126 and geniposide
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Geniposide suppresses LPS-induced nitric oxide, PGE2 and inflammatory cytokine by downregulating NF-κB, MAPK and AP-1 signaling pathways in macrophages.
Inflammatory responses are important to host immune reactions, but uncontrolled inflammatory mediators may aid in the pathogenesis of other inflammatory diseases. Geniposide, an iridoid glycoside found in the herb gardenia, is believed to have broad-spectrum anti-inflammatory effects in murine models but its mechanism of action is unclear. We investigated the action of this compound in murine macrophages stimulated by lipopolysaccharide (LPS), as the stimulation of macrophages by LPS is known to induce inflammatory reactions. We determined the effect of geniposide on LPS-induced production of the inflammatory mediators, nitric oxide (NO) and prostaglandin E2 (PGE2), the mRNA and protein expression of the NO and PGE2 synthases, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), respectively, and the mRNA and protein expression of the inflammatory cytokine, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Furthermore, nuclear factor (NF)-κB, mitogen-activated protein kinase (MAPK) and activator protein (AP)-1 activity were assayed. To understand the action of geniposide on the NF-κB and MAPK pathways, we studied the effect of NF-κB and MAPK inhibitors on the LPS-induced production of NO, PGE2 and TNF-α. Our findings clearly showed that geniposide mainly exerts its anti-inflammatory effects by inhibiting the LPS-induced NF-κB, MAPK and AP-1 signaling pathways in macrophages, which subsequently reduces overexpression of the inducible enzymes iNOS and COX-2 and suppresses the expression and release of the inflammatory factors, TNF-α, IL-6, NO and PGE2. Thus, geniposide shows promise as a therapeutic agent in inflammatory diseases. Topics: Animals; Anti-Inflammatory Agents; Butadienes; Cell Line; Cyclooxygenase 2; Dinoprostone; Extracellular Signal-Regulated MAP Kinases; Gardenia; Imidazoles; Inflammation Mediators; Interleukin-6; Iridoids; Lipopolysaccharides; Macrophages, Peritoneal; Male; Mice; Mice, Inbred Strains; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; Nitriles; Pyridines; Signal Transduction; Sulfones; Transcription Factor AP-1; Tumor Necrosis Factor-alpha | 2014 |
Neurotrophic property of geniposide for inducing the neuronal differentiation of PC12 cells.
The emerging data show that the insulinotrophic hormone glucagon-like peptide-1(GLP-1) and its agonist extendin-4 have neurotrophic function to inducing neuronal differentiation of PC12 cells and prevent neurons damage challenged by oxidative stress. Here, with the model of high throughput screen for GLP-1 receptor agonists, we screen and identify that geniposide is a novel agonist for GLP-1 receptor. Furthermore, geniposide induces the neuronal differentiation of PC12 cells with resulting neurites outgrowth; we also observe an increase in expression of growth-associated protein-43. U0126, a selective MEK inhibitor, prevents neurites out growth and phosphorylation of mitogen-activated kinase proteins in PC12 cells induced by geniposide. All these results show that activation of GLP-1 receptor by geniposide to induce the neuronal differentiation of PC12 cells involves in MAPK signaling cascade. Topics: Animals; Blotting, Western; Butadienes; Cell Differentiation; Cell Line; Colforsin; Dose-Response Relationship, Drug; Drug Interactions; Enzyme Inhibitors; GAP-43 Protein; Gene Expression; Glucagon-Like Peptide 1; Glucagon-Like Peptide-1 Receptor; Humans; Iridoids; Luciferases; Mitogen-Activated Protein Kinase Kinases; Nerve Growth Factor; Neurons; Neuroprotective Agents; Nitriles; PC12 Cells; Pyrans; Rats; Receptors, Glucagon; Transfection | 2006 |