Irsogladine, an anti-ulcer drug, suppresses superoxide production by inhibiting phosphodiesterase type 4 in human neutrophils.

  title={Irsogladine, an anti-ulcer drug, suppresses superoxide production by inhibiting phosphodiesterase type 4 in human neutrophils.},
  author={Takashi Kyoi and Kumiko Noda and Michiko Oka and Yojiro Ukai},
  journal={Life sciences},
  volume={76 1},

Imperatorin alleviates psoriasiform dermatitis by blocking neutrophil respiratory burst, adhesion, and chemotaxis through selective PDE4 inhibition.

Imperatorin is a natural inhibitor of PDE4A/B/C and may serve as a lead for developing new therapeutics to treat neutrophilic psoriasis and inhibit Akt, ERK, JNK, and Ca2+ mobilization.

Aryl-1,3,5-triazine ligands of histamine H4 receptor attenuate inflammatory and nociceptive response to carrageen, zymosan and lipopolysaccharide

The results demonstrate the anti-inflammatory and analgesic activity of the new aryl-1,3,5-triazine derivatives, which are primarily H4R–dependent.

Irsogladine maleate suppresses indomethacin-induced elevation of proinflammatory cytokines and gastric injury in rats.

The mucosal protective effects afforded by irsogladine maleate on gastric injury induced by indomethacin are mediated by inhibition of mucosal proinflammatory cytokine production and neutrophil infiltration, leading to suppression of mucosa inflammation and subsequent tissue destruction.

Aggravation by Paroxetine, a Selective Serotonin Reuptake Inhibitor, of Antral Lesions Generated by Nonsteroidal Anti-Inflammatory Drugs in Rats

It is suggested that SSRIs aggravate NSAID-induced antral lesions, probably via the activation of 5HT3 receptors, and the mechanism of aggravation may involve the corrosive action of acid/pepsin as well as an impaired antioxidative system.



Anti-Oxidative Effects of Theophylline on Human Neutrophils Involve Cyclic Nucleotides and Protein Kinase A

The beneficial, anti-inflammatory interactions of theophylline with human nuetrophils are related to the phosphodiesterase inhibitory properties of this agent, and are selective for those pro-inflammatory stimuli which elevate cAMP, resulting in enhanced activity of protein kinase A and inhibition of the production of potentially harmful reactive oxidants by these cells.

Suppression of human eosinophil respiratory burst and cyclic AMP hydrolysis by inhibitors of type IV phosphodiesterase: interaction with the beta adrenoceptor agonist albuterol.

The data suggest that cyclic AMP levels in human eosinophils are regulated by the action of a type IV PDE isoenzyme and that elevation of the intracellular cyclicAMP concentration by PDE IV inhibition can suppress the functional activity of these cells.

Irsogladine prevents monochloramine-induced gastric mucosal lesions by improving the decrease in mucosal blood flow due to the disturbance of nitric oxide synthesis in rats.

It is suggested that the improvement of the decrease in mucosal blood flow subsequent to the disturbance of gastric nitric oxide synthesis is involved in the protective effect of irsogladine on gastric mucosal lesions caused by NH(2)Cl.

Stimulus-dependent inhibition of superoxide generation by prostaglandins.

Polymorphonuclear leukocyte inhibition by therapeutic concentrations of theophylline is mediated by cyclic-3',5'-adenosine monophosphate.

Theophylline inhibition of PMN function appeared to be associated with both an increase in cAMP and a decrease in intracellular calcium, which may be relevant to both the therapeutic and adverse pharmacologic actions of theophyllines.

Gastric ulceration induced by nonsteroidal anti-inflammatory drugs is a neutrophil-dependent process.

An important role for neutrophils in the pathogenesis of NSAID-induced gastric ulceration is suggested and may be important in the vascular injury that occurs early after administration of these compounds.

Formation of reactive oxygen metabolites in glomeruli is suppressed by inhibition of cAMP phosphodiesterase isozyme type IV.

It is suggested that selective inhibitor of PDE-IV rolipram acted via the cAMP-signaling pathway and suppressed ROM generation possibly via phosphorylating ras-type GTP-binding protein component of NADPH oxidase and thereby blocking assembly of functional NADPH oxidation complex.