BACKGROUND: The flowers of Inula japonica (Inulae Flos) have long been used in traditional medicine for the treatment of inflammatory diseases. In the present study, we investigated the anti-inflammatory properties of Inulae Flos Extract (IFE). METHODS: The anti-inflammatory effects of IFE against nitric oxide (NO), PGE2, TNF-alpha, and IL-6 release, as well as NF-kappa B and MAP kinase activation were evaluated in RAW 264.7 cells. RESULTS: IFE inhibited the production of NO and the expression of inducible nitric oxide synthase (iNOS) in LPS-stimulated RAW264.7 cells. In addition, IFE reduced the release of pro-inflammatory cytokines, such as TNF-alpha and IL-6. Furthermore, IFE inhibited the NF-kappa B activation induced by LPS, which was associated with the abrogation of I kappa B-alpha degradation and subsequent decreases in nuclear p65 and p50 levels. Moreover, the phosphorylation of ERK, JNK, and p38 MAP kinases in LPS-stimulated RAW 264.7 cells was suppressed by IFE in a dose-dependent manner. CONCLUSION: These results suggest that the anti-inflammation activities of IFE might be attributed to the inhibition of NO, iNOS and cytokine expression through the down-regulation of NF-kappa B activation via suppression of I kappa B alpha and MAP kinase phosphorylation in macrophages.
Cytokines ; Dinoprostone ; Down-Regulation ; Flowers ; I-kappa B Proteins ; Interleukin-6 ; Inula ; Macrophages ; Medicine, Traditional ; NF-kappa B ; Nitric Oxide ; Nitric Oxide Synthase Type II ; Phosphorylation ; Phosphotransferases ; Tumor Necrosis Factor-alpha

A 60-year-old man with biliary ascariasis accompanied by choledocholithiasis and biliary pancreatitis, is herein reported. His chief complaints were epigastric pain, nausea, and vomiting. He had a past history of eating raw fish and vegetables. An endoscopic retrograde cholangiopancreatography (ERCP) revealed multiple CBD stones and a live ascaris adult worm in the common bile duct which was not detected by an abdominal CT. The management of biliary obstruction caused by Ascaris lumbricoides has usually been surgical, but this report describes the endoscopic removal of the ascaris located in the common bile duct.
Adult ; Ascariasis* ; Ascaris ; Ascaris lumbricoides ; Cholangiopancreatography, Endoscopic Retrograde ; Choledocholithiasis* ; Common Bile Duct ; Eating ; Humans ; Middle Aged ; Nausea ; Pancreatitis* ; Tomography, X-Ray Computed ; Vegetables ; Vomiting

Rac1 and Rac2 are essential for the control of oxidative burst catalyzed by NADPH oxidase. It was also documented that Rho is associated with the superoxide burst reaction during phagocytosis of serum- (SOZ) and IgG-opsonized zymosan particles (IOZ). In this study, we attempted to reveal the signal pathway components in the superoxide formation regulated by Rho GTPase. Tat-C3 blocked superoxide production, suggesting that RhoA is essentially involved in superoxide formation during phagocytosis of SOZ. Conversely SOZ activated both RhoA and Rac1/2. Inhibition of RhoA-activated kinase (ROCK), an important downstream effector of RhoA, by Y27632 and myosin light chain kinase (MLCK) by ML-7 abrogated superoxide production by SOZ. Extracellular signaling-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) were activated during phagocytosis of SOZ, and Tat-C3 and SB203580 reduced ERK1/2 and p38 MAPK activation, suggesting that RhoA and p38 MAPK may be upstream regulators of ERK1/2. Inhibition of ERK1/2, p38 MAPK, phosphatidyl inositol 3-kinase did not block translocation of RhoA to membranes, suggesting that RhoA is upstream to these kinases. Inhibition of RhoA by Tat-C3 blocked phosphorylation of p47 PHOX. Taken together, RhoA, ROCK, p38MAPK, ERK1/2, and p47 PHOX may be subsequently activated, leading to activation of NADPH oxidase to produce superoxide.
Animals ; Cell Line ; Cell Membrane ; Cytosol ; Enzyme Inhibitors/pharmacology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Macrophage-1 Antigen/pharmacology ; Macrophages/drug effects/*metabolism/ultrastructure ; Mice ; Myosin-Light-Chain Kinase/metabolism ; Opsonin Proteins/blood/*metabolism ; *Phagocytosis ; Protein Transport ; Protein-Serine-Threonine Kinases/metabolism ; Research Support, Non-U.S. Gov't ; *Signal Transduction ; Superoxides/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Zymosan/*blood ; p38 Mitogen-Activated Protein Kinases/metabolism ; rhoA GTP-Binding Protein/antagonists & inhibitors/*metabolism