Antinociceptive activity of fractions from Couroupita guianensis Aubl. leaves.
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BACKGROUND
Couroupitaguianensis Aubl. (Lecythidaceae) is popularly known in Brazil as "abricó-de-macaco". Infusions or teas obtained from its leaves, flowers, and barks are used in South America for the treatment of several disorders such as pain and inflammatory processes.
OBJECTIVE
Evaluate antinociceptive effects of crude ethanol extract (CEE) and its fractions in three analgesic models (acetic acid-induced contortions, tail flick, and hot plate) and study the possible mechanism of their action.
METHODS
CEE, hexane, dichloromethane, ethyl acetate, and butanol fractions (10, 30, and 100mg/kg, p.o.) and the reference drug morphine (5mg/kg, s.c.) were evaluated. To elucidate the mechanism of action from the fractions, animals were pre-treated (30 min) with atropine (muscarinic receptor antagonist, 1mg/kg, s.c.), mecamylamine (nicotinic receptor antagonist, 2mg/kg, s.c.), naloxone (opioid receptor antagonist, 1mg/kg, s.c.) or L-nitro arginine methyl ester (L-NAME, nitric oxide synthase inhibitor, 3mg/kg, s.c.).
RESULTS
CEE and fractions significantly inhibited the number of contortions induced by acetic acid. All fractions showed antinociceptive activity in the tail flick model, being the hexane and ethyl acetate the most potent and long acting fractions. In the hot plate method the highest effect observed was at the dose of 100mg/kg from all fractions. Administration of naloxone inhibited the antinociceptive effect of fractions. Pre-treatment of mice with atropine reduced the antinociceptive activity of CEE and its fractions, the exception being the dichloromethane fraction. Mecamylamine did not inhibited the effect of dichloromethane fraction. L-NAME reduced the anti-hyperalgesic effect of all fractions, but the most prominent effect was observed in the antinociceptive activity caused by CEE and butanol fraction.
CONCLUSIONS
Results obtained demonstrated that Couroupita guianensis CEE and its fractions have antinociceptive activity that is mediated, at least in part, by opioid and cholinergic systems and nitric oxide pathway.
