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Abstract
The venoms of Bothrops asper (BaV) and Bothrops jararaca (BjV), two of the most medically
important poisonous snakes of Latin America, cause pronounced oedema in the victims
through poorly understood mechanisms. In the present study, we examined the possible
role of cyclooxygenases (COX) in the genesis of mouse paw oedema caused by BaV and
BjV injections. BaV at 2.5 microg/paw and BjV at 0.75 microg/paw induced significant
oedema that persisted for up to 6h following subplantar injection. Treatment with
indomethacin (2 mg/kg), rofecoxib, (10 mg/kg), or dexamethasone (2 mg/kg) significantly
reduced the BaV- and BjV-induced oedema formation. Treatment with SC-560 (30 mg/kg)
significantly reduced the oedema formation induced by BjV but had no effect on that
induced by BaV. Both venoms induced significant increases in the levels of prostaglandin
E(2) (PGE(2)) and the expression of COX-1 and COX-2 in paw tissue. The peak of oedema
formation and PGE(2) release correlated with marked expression of COX-2 in the paw
tissue. These results demonstrate that injection of BaV and BjV results in a rapid
increase in oedema formation that is, at least partially, mediated by arachidonic
acid metabolites formed by COX-2. In the case of BjV, COX-1-derived prostanoids also
appear to contribute significantly to the inflammatory changes.