Assessment of the antiexudative and antiproliferative activities of non-steroidal anti-inflammatory drugs in inflammatory models developed in rats by subcutaneous implantation of bacterial cell walls from the dental plaque.
A purified bacterial cell walls suspension from human dental plaque were biochemically prepared to serve as flogogenous agent in producing experimental inflammatory models in rats. In the vascular permeability inhibition assay (edemogenic test), the subcutaneous implantation of the flogogenous agent elicited an acute inflammatory reaction highly susceptible to the effects of the non-steroidal anti-inflammatory drugs (NSAIDs). The intradermal injection of the flogogenous agent in the dorsum of rats developed experimental granulomas also susceptible to the anti-inflammatory effects of the NSAIDs. Otherwise, the antimitotic effect of drugs was carried out in the model of cellular proliferation of duodenal mucosa of rats by incorporation of tritiated thymidine (3H TdR) in the DNA. These models of acute and chronic inflammation, and the antimitotic model permitted us to evaluate the anti-inflammatory and antimitotic effects of sulindac, ibuprofen, naproxen and glucametacin. In the antiexudative activity, evaluated by the edemogenic test, naproxen was the more effective drug followed by sulindac, ibuprofen and glucametacin (in a decreasing order of potency) to inhibit the exudative response induced by the bacterial cell walls suspension, in all experimental periods. In the chronic anti-inflammatory activity, evaluated by the granuloma inhibition assay, all drugs were capable to demonstrate effectiveness against the development of the experimental granulomas induced by an intradermal injection of the flogogenous agent. In the model of cellular proliferation, all tested drugs demonstrated antimitotic activity in all experimental periods (4, 6 and 8 days), also. Sulindac induced the higher antimitotic effect, in all experimental periods, followed by ibuprofen, naproxen and glucametacin in a decreasing order of efficacy. There was a positive correlation between the antiexudative, anti-proliferative, and antimitotic effects.
Guimarães
S A
SA
Department of Pathology, School of Dentistry of Bauru, University of São Paulo, Brazil.
Akatsu
T
T
Tago
E M
EM
Consolaro
A
A
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D002199:Capillary Permeability / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002473:Cell Wall; D002648:Child; D004261:DNA Replication / Q000187:drug effects; D003773:Dental Plaque / Q000382:microbiology*; D004386:Duodenum; D004487:Edema / Q000209:etiology / Q000517:prevention & control; D005122:Exudates and Transudates; D006099:Granuloma / Q000209:etiology / Q000517:prevention & control; D006131:Growth Inhibitors / Q000494:pharmacology*; D006801:Humans; D007052:Ibuprofen / Q000494:pharmacology / Q000627:therapeutic use; D007213:Indomethacin / Q000031:analogs & derivatives / Q000494:pharmacology / Q000627:therapeutic use; D007249:Inflammation / Q000188:drug therapy* / Q000473:pathology; D007413:Intestinal Mucosa / Q000187:drug effects; D009288:Naproxen / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D013467:Sulindac / Q000494:pharmacology / Q000627:therapeutic use
D000894:Anti-Inflammatory Agents, Non-Steroidal; D006131:Growth Inhibitors; D013467:Sulindac; D009288:Naproxen; C010581:glucametacin; D007052:Ibuprofen; D007213:Indomethacin