benzofurans has been researched along with triptolide* in 2 studies
1 review(s) available for benzofurans and triptolide
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Recent pharmacological studies on natural products in China.
Natural products have been used as medicinal agents for many years. In addition, these compounds have also served as the starting points for semisynthetic analogs with improved properties. This review focuses on recent advances in the pharmacological studies on natural products mainly performed and published in China. Emphasis will be placed on those compounds that show the greatest promise clinically such as huperzine A (9-amino-13-ethylidene-11-methyl-4-azatricyclo[7.3.1.0(3.8)]trideca-3(8),6,11-trien-5-one), s-(-)-3-n-butylphthalide (s-(-)-3-butyl-1(3H)-isobenzofuranone), (-)-clausenamide (3-hydroxy-4-phenyl-5a-hydroxybenzyl-N-methyl-gamma-lactam) and Ginkgo biloba extract and its active components. Topics: Alkaloids; Animals; Benzofurans; Berberine; China; Cholinesterase Inhibitors; Diterpenes; Dopamine Agonists; Dopamine Antagonists; Drugs, Chinese Herbal; Epoxy Compounds; Ginkgo biloba; Humans; Immunosuppressive Agents; Lactams; Lignans; Neuroprotective Agents; Phenanthrenes; Rutaceae; Sesquiterpenes | 2004 |
1 other study(ies) available for benzofurans and triptolide
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Anti-inflammatory effects of mapracorat, a novel selective glucocorticoid receptor agonist, is partially mediated by MAP kinase phosphatase-1 (MKP-1).
Mapracorat is a novel selective glucocorticoid receptor agonist (SEGRA), structurally distinct from corticosteroids. In preclinical studies, mapracorat potently inhibits the production of a variety of inflammatory mediators including cytokines and prostaglandin E2 (PGE(2)), with limited side effects associated with traditional corticosteroids. The objective of this study was to delineate the mechanisms underlying the anti-inflammatory properties of mapracorat. We found that mapracorat potently inhibited the production of GM-CSF and TNF-α in LPS-stimulated Raw 264.7 macrophages. Mapracorat also substantially attenuated the expression of COX-2 and the production of PGE(2). The inhibition of mapracorat on the inflammatory response was dose-dependent, and substantially inhibitory effects were observed at concentrations in the 10-100 nm range. Examination of the activation kinetics of p38 and its downstream target MAPK-activated protein kinase-2 (MK-2) revealed a shortened activation course after LPS stimulation in cells pretreated with mapracorat. Supporting the notion that mapracorat augments a feedback control mechanism restraining the p38 pathway, we found that mapracorat enhanced the expression of MAPK phosphatase-1 (MKP-1), a critical negative regulator of MAPKs that drive the production of cytokines and other inflammatory mediators. While mapracorat alone did not stimulate MKP-1 expression, it markedly enhanced the expression of MKP-1 in cells stimulated by LPS, in a similar manner and potency to the augmenting effect of dexamethasone. Blocking MKP-1 expression by triptolide also abolished the accelerating effects of mapracorat on p38 and MK-2 deactivation, further supporting a role of MKP-1 in the anti-inflammatory mechanism of mapracorat. Taken together, these results indicate that mapracorat exerts its anti-inflammatory effects, at least in part, by augmenting MKP-1 expression. Topics: Animals; Anti-Inflammatory Agents; Antineoplastic Agents, Alkylating; Benzofurans; Cell Line; Dexamethasone; Diterpenes; Dose-Response Relationship, Drug; Dual Specificity Phosphatase 1; Epoxy Compounds; Gene Expression Regulation, Enzymologic; Granulocyte-Macrophage Colony-Stimulating Factor; Intracellular Signaling Peptides and Proteins; Lipopolysaccharides; Macrophages; Mice; p38 Mitogen-Activated Protein Kinases; Pentanols; Phenanthrenes; Protein Serine-Threonine Kinases; Quinolines; Receptors, Glucocorticoid; Tumor Necrosis Factor-alpha | 2012 |