The mechanism of croton oil-induced inflammation involves
an increase in phospholipase A-2 activity (Kondoh et al., 1985;
McColl et al., 1986), which in turn leads to the release of arachidonic
acid and subsequent biosynthesis of leukotrienes and
prostaglandins (Ashendel and Boutwell, 1979; Furstenberger
and Marks, 1980), which also involves the lipooxygenase pathway.
Arachidonic acid metabolites have been firmly shown to
act as mediators of the inflammatory response via cyclooxygenase
and lipooxygenase activity, and have therefore been a
target for the development of therapeutic agents (Inoue et al.,
1989).
The lack of an inhibitory effect of the hydroalcoholic extract
on pleurisy, in contrast to the inhibitory effect on ear edema,
may be attributable to several factors, including the action of the
extract on the different inflammatory mediators involved in the
models studied. Differences in the process of absorption of the
extract must also be considered and are related to the different
routes of administration (oral and topical). In this context, we
cannot discount the possibility of irregular absorption after oral
administration