Abstract
BackgroundPlants rich in flavonoids, such as açaí (Euterpe oleraceae Mart.), can induce antinociception in experimental animals. Here, we tested an extract obtained from the stones of açaí fruits (açaí stone extract, ASE), a native plant from the Amazon region of Brazil, in models of acute/inflammatory and chronic pain.MethodsAntinociceptive effects of ASE were evaluated in the hot plate, formalin, acetic acid writhing, carrageenan, and neuropathic pain models, as well as in thermal hyperalgesia and mechanical allodynia models induced by spinal nerve ligation. Antinociceptive activities were modulated by the administration of cholinergic, adrenergic, opioid, and L-arginine-NO antagonists.ResultsOral administration of ASE (30, 100, or 300 mg.kg−1) dose-dependently reduced nociceptive responses to acute/inflammatory pain in mice, including thermal hyperalgesia, acetic acid-induced writhing, and carrageenan-induced thermal hyperalgesia. Moreover, ASE reduced the neurogenic and inflammatory phases after intraplantar injection of formalin in mice. The antinociceptive effect of ASE (100 mg · kg−1) in a hot plate protocol, was inhibited by pre-treatment with naloxone (1 mg · kg−1), atropine (2 mg · kg−1), yohimbine (5 mg · kg−1), or L-NAME (30 mg · kg−1). Furthermore, ASE prevented chronic pain in a rat spinal nerve ligation model, including thermal hyperalgesia and mechanical allodynia.ConclusionASE showed significant antinociceptive effect via a multifactorial mechanism of action, indicating that the extract may be useful in the development of new analgesic drugs.
Highlights
MethodsAntinociceptive effects of ASE were evaluated in the hot plate, formalin, acetic acid writhing, carrageenan, and neuropathic pain models, as well as in thermal hyperalgesia and mechanical allodynia models induced by spinal nerve ligation
Plants rich in flavonoids, such as açaí (Euterpe oleraceae Mart.), can induce antinociception in experimental animals
Inhibition of NO synthesis antagonizes the activities of several antinociceptive compounds [28]. These results indicate that ASE has an antinociceptive effect that is modulated by the cholinergic, adrenergic, opioid, and L-arginine-NO pathways
Summary
E. oleracea Mart. fruits (açaí) were obtained from Amazon Bay (Belém do Pará, Brazil; excicata number 29052, Museu Goeldi-Belem do Pará). Withdrawal latency (reaction time of the animal when placed on a surface heated to 52 °C) was measured before and 30 min after oral administration of either saline tramadol (2 mg.kg−1) or ASE (30, 100 or 300 mg.kg−1). Formalin (2.5 %, 20 μl) was administered by intraplantar injection into the right hind paw 15 min after oral administration of saline, acetylsalicylic acid Inhibition of muscarinic receptors by atropine reduced, but did not abolish the antinociceptive effect of ASE This finding suggests that cholinergic mechanisms may mediate these activities. Inhibition of NO synthesis antagonizes the activities of several antinociceptive compounds [28] Taken together, these results indicate that ASE has an antinociceptive effect that is modulated by the cholinergic, adrenergic, opioid, and L-arginine-NO pathways. Reactivity in the neurogenic phase was not affected by oral administration of the lowest doses of ASE (30 mg.kg−1) or acetylsalicylic acid (150 mg.kg−1), but was reduced by higher doses (100 and 300 mg.kg−1 ASE) to 45.6 ± 5.0 s and Acetylsalicylic acid 150 mg.kg-1
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