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

Sudo RT, Neto ML, Monteiro CE, Amaral RV, Resende ÂC, Souza PJ, Zapata-Sudo G, Moura RS - BMC Complement Altern Med (2015)

Bottom Line: 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)).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.

View Article: PubMed Central - PubMed

Affiliation: Program of Research in Drug Development, Institute of Biomedical Science, Federal University of Rio de Janeiro, UFRJ, Brazil. Av. Carlos Chagas Filho, 373 - Centro de Ciências da Saúde - bloco J, sala 14. Cidade Universitária - Ilha do Fundão, Rio de Janeiro, 21941-902, Brazil. rtsudo@icb.ufrj.br.

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.

No MeSH data available.


Related in: MedlinePlus

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
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4489033&req=5

Fig1: 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

Mentions: The hot plate test in mice [12] was used to test the effect of orally administered ASE (30, 100 or 300 mg.kg−1) on pain responses mediated by the central nervous system (CNS). Oral tramadol (2 mg.kg−1) was used as a positive control. 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). Additional measurements were performed every 15 min up to 120 min to determine the maximum possible effect (%MPE), which occurred 20–25 min after ASE administration. Analgesic activity was calculated as the %MPE by using the formula: %MPE = [(latency observed) – (latency control) x 100] / [(cut-off) – (latency control)] (Fig. 1).Fig. 1


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

Sudo RT, Neto ML, Monteiro CE, Amaral RV, Resende ÂC, Souza PJ, Zapata-Sudo G, Moura RS - BMC Complement Altern Med (2015)

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
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4489033&req=5

Fig1: 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
Mentions: The hot plate test in mice [12] was used to test the effect of orally administered ASE (30, 100 or 300 mg.kg−1) on pain responses mediated by the central nervous system (CNS). Oral tramadol (2 mg.kg−1) was used as a positive control. 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). Additional measurements were performed every 15 min up to 120 min to determine the maximum possible effect (%MPE), which occurred 20–25 min after ASE administration. Analgesic activity was calculated as the %MPE by using the formula: %MPE = [(latency observed) – (latency control) x 100] / [(cut-off) – (latency control)] (Fig. 1).Fig. 1

Bottom Line: 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)).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.

View Article: PubMed Central - PubMed

Affiliation: Program of Research in Drug Development, Institute of Biomedical Science, Federal University of Rio de Janeiro, UFRJ, Brazil. Av. Carlos Chagas Filho, 373 - Centro de Ciências da Saúde - bloco J, sala 14. Cidade Universitária - Ilha do Fundão, Rio de Janeiro, 21941-902, Brazil. rtsudo@icb.ufrj.br.

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.

No MeSH data available.


Related in: MedlinePlus