Abstract
Objective: was to examine agar as a phlogistic agent in the air pouch model. Method and Materials: Rats were divided into five groups and the effects of 1%, 2%, 3% and 4% agar in the air pouch model were compared with those of 1% carrageenan. The vascular inflammation induced by agar and the microvasculature of the air pouch membrane were analysed. In addition, the role of nitric oxide (NO)-dependent pathways and cellular migration in the responses to 2% agar were evaluated. To assess the mechanism of action underlying the inflammatory effects of agar, rats were treated with a standard anti-inflammatory drug, either celecoxib or acetylsalicylic acid. In addition, a differential leucocyte cell count, total cell count and NO and PGE2 concentrations were determined. Results: The 2% agar was chosen as the optimal concentration. Celecoxib or ASA both inhibited the inflammatory effects of agar, reducing the area of the microvasculature in the tissue lining the air pouch, as well as NO and PGE2 concentrations and cell migration in the exudate. Conclusion: The present study shows that a simple and alternative method (agar) produces consistent results in the air pouch model and can be used as an alternative experimental model of inflammation.
Highlights
Inflammation is the response of an organism to an injurious stimulus that initiates healing (Kenneth and Hajime, 2008)
To assess the mechanism of action underlying the inflammatory effects of agar, rats were treated with a standard antiinflammatory drug, either celecoxib or acetylsalicylic acid
4% agar increased the number of ischaemic points and a foul odour was noted after opening the air pouch in this treatment group
Summary
Inflammation is the response of an organism to an injurious stimulus that initiates healing (Kenneth and Hajime, 2008). There are many mechanisms involved in inflammatory responses to infections, chronic diseases and other tissue injuries. This variety and the search for new anti-inflammatory drugs with higher specificity and fewer side-effects justify the development of new protocols and standardization of experimental inflammatory models (Kenneth and Hajime, 2008). The air pouch model was developed as an in vivo bioassay in rodents modelling a typical inflamed system (Bastos et al, 2008; Tao et al, 1999). The air pouch model of inflammation is widely used because it produces localized effects and is easy to create. The model enables easy collection of any inflammatory cells produced, as well as measurement of chemotaxis and the production of inflammatory chemical mediators (Bastos et al, 2008; Tao et al, 1999)
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