Pharmacological Demonstration of Inflammatory Mediators Using Experimental Inflammatory Models: Rat Pleurisy Induced by Carrageenin and Phorbol Myristate Acetate

Abstract

Rat pleurisy induced by carrageenin or phorbol myristate acetate (PMA) was utilized for examination of the plasma exudation process of inflammation. Chemical mediators responsible for induction of vascular permeability increase were examined. In carrageenin-induced pleurisy, kinin and PGI₂ were demonstrated as the main mediators, and in PMA pleurisy histamine, PGI₂ and platelet-activating factor were the main mediators. These results indicate that different stimuli may activate different enzymatic processes to produce different mediators, but they may result in similar inflammatory reactions by action of these multiple mediators simultaneously released.

Protective effect of gastrin-releasing peptide receptor antagonist in carrageenan-induced pleural inflammation in rats

“…There is a large amount of evidence that the enhanced formation of nitric oxide (NO) by inducible nitric oxide synthase (NOS) may negatively contribute to the inflammatory process [3,[31][32][33][34]. For instance, inhibitors of NOS activity reduce the development of carrageenan-induced inflammation [32,35].…”

Effect of total phenolics from Laggera alata on acute and chronic inflammation models

“…derived mediators (Oh-ishi et al, 1989;Dawson et al, 1991;Peskar et al, 1991;Cuzzocrea et al, 1997). In addition to oxyradicals, overproduction of NO also plays an important role in various models of inflammation (Moncada et al, 1991;Nanthan, 1996;Cuzzocrea et al, 1998).…”

Evaluation of antiinflammatory activity of the total flavonoids of Laggera pterodonta on acute and chronic inflammation models

“…It has been reported that in the process of carrageenan-induced inflammation, the early phase is related to the production of histamine, leukotrienes, platelet-activating factor and possibly cyclooxygenase products, while the delayed phase is linked to neutrophil infiltration and the production of neutrophil-derived free radicals, such as hydrogen peroxide, superoxide and hydroxyl radicals, as well as to the release of other neutrophil-derived mediators (Oh-ishi et al, 1989;Dawson et al, 1991). In addition to oxyradicals, overproduction of NO also plays an important role in various models of inflammation (Cuzzocrea et al, 1998;Moncada et al, 1991).…”