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. 2015 Jul 2:15:208.
doi: 10.1186/s12906-015-0724-2.

Antinociceptive effects of hydroalcoholic extract from Euterpe oleracea Mart. (Açaí) in a rodent model of acute and neuropathic pain

Affiliations

Antinociceptive effects of hydroalcoholic extract from Euterpe oleracea Mart. (Açaí) in a rodent model of acute and neuropathic pain

Roberto T Sudo et al. BMC Complement Altern Med. .

Abstract

Background: Plants 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.

Methods: Antinociceptive 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.

Results: Oral 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.

Conclusion: ASE showed significant antinociceptive effect via a multifactorial mechanism of action, indicating that the extract may be useful in the development of new analgesic drugs.

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Figures

Fig. 1
Fig. 1
a Effect of ASE (30, 100 and 300 mg.kg−1, p.o.) and tramadol (2 mg.kg−1, p.o) in the hot plate test, b Evaluation of mechanism of action of ASE. The bars represent the mean ± SEM (n = 10). *P < 0.05 versus saline, # P < 0.05 versus ASE group. ANOVA followed by Newman-Keuls test
Fig. 2
Fig. 2
Effect of ASE and acetylsalicylic acid on the formalin test. The bars represent mean ± SEM (n = 10). *P < 0.05 versus saline. ANOVA followed by Newman-Keuls test
Fig. 3
Fig. 3
Effect anti-hyperalgesic of ASE and acetylsalicylic acid on the carrageenan test. The points represent the mean ± SEM (n = 10). *P < 0.05 versus saline. Two-way ANOVA followed by Bonferroni post hoc test
Fig. 4
Fig. 4
Effect of ASE and indomethacin on the acetic acid-induced writhing test. The number of writhing was evaluated during 30 minutes. The bars represent the mean ± SEM (n = 10). *P < 0.05 versus saline. ANOVA followed by Newman-Keuls test
Fig. 5
Fig. 5
Antinociceptive effect of ASE or amitriptyline in SNL rats. The ASE and amitriptyline were once daily administered by gavage during 7 days. a) Latency in response to thermal stimulation and b) Withdrawal threshold in response to mechanical stimulation applied to the paw of rats submitted to SNL. The points represent the mean ± SEM (n = 4). *P < 0.05 versus day 0; # P < 0.05 versus day 7. Two-way ANOVA followed by Bonferroni post hoc test

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