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. 2013 Jul;113(1):1-7.
doi: 10.1111/bcpt.12051. Epub 2013 Feb 25.

Antinociceptive and anti-inflammatory activities of the ethanolic extract, fractions and 8-methoxylapachenol from Sinningia allagophylla tubers

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Free article

Antinociceptive and anti-inflammatory activities of the ethanolic extract, fractions and 8-methoxylapachenol from Sinningia allagophylla tubers

Felipe L Barbosa et al. Basic Clin Pharmacol Toxicol. 2013 Jul.
Free article

Abstract

This study investigated the antinociceptive and anti-inflammatory activities of the ethanolic extract (EESAl), fractions and the compound 8-methoxylapachenol (8ML) obtained from the tubers of Sinningia allagophylla. Male Swiss mice were treated with EESAl (3-300 mg/kg) or vehicle by oral route (p.o.) 1 hr before the injection of formalin 2.5% or carrageenan (Cg) into the hind paw. EESAl (3-30 mg/kg) reduced the inflammatory phase of the nociceptive behaviour induced by formalin (around 65% for all doses). EESAl (3-300 mg/kg, p.o.) also reduced Cg-induced mechanical hyperalgesia and oedema in a dose-dependent fashion but did not change the hot-plate latency or the motor performance of the animals. Oral administration of petroleum ether fraction (PE, 3 mg/kg), but not in the methanolic fraction (30 mg/kg), reduced both Cg-induced oedema and hyperalgesia. Compound 8ML isolated from PE (1.8 mg/kg, p.o.) abolished Cg-induced hyperalgesia but also did not change hot-plate latency or motor performance of the animals. 8ML administration into the paw (0.75-750 pg) dose-dependently reduced Cg-induced hyperalgesia. 8ML (750 pg) also blocked the hyperalgesia induced by tumour necrosis factor (TNF-α), interleukin-1β (IL-1β) and prostaglandin E2 (PGE2 ) but failed to change the hyperalgesia induced by cytokine-induced neutrophil chemoattractant-1 (CINC-1) and dopamine (Dopa). These results suggest that EESAl has an important antinociceptive and anti-inflammatory activity, the former one related, at least in part, to the reduction in the hyperalgesia. Similarly, 8ML reduced Cg-induced oedema and mechanical hyperalgesia and seems to act in peripheral sites and on the prostaglandin rather than on the sympathetic component of the Cg-inflammatory hyperalgesia.

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