Author(s):
Maia, Juliana Lemos ; Lima Júnior, Roberto César Pereira ; Melo, Caroline Mourão ; David, Juceni Pereira de Lima ; David, Jorge Mauricio ; Campos, Adriana Rolim ; Santos, Flávia Almeida ; Rao, Vietla Satyanarayana ; Maia, Juliana Lemos ; Lima Júnior, Roberto César Pereira ; Melo, Caroline Mourão ; David, Juceni Pereira de Lima ; David, Jorge Mauricio ; Campos, Adriana Rolim ; Santos, Flávia Almeida ; Rao, Vietla Satyanarayana
Date: 2012
Origin: Oasisbr
Subject(s): Oleanolic acid; Pentacyclic triterpene; Capsaicin; Antinociceptive activity; Endogenous opioids; Nitric oxide; KATP-channels
Description
RESTRITO
Submitted by Santiago Fabio (fabio.ssantiago@hotmail.com) on 2012-07-10T14:48:21Z No. of bitstreams: 1 DD.pdf: 191921 bytes, checksum: e7e0d97358e281aeda5710f62c757522 (MD5)
Made available in DSpace on 2012-07-10T14:48:21Z (GMT). No. of bitstreams: 1 DD.pdf: 191921 bytes, checksum: e7e0d97358e281aeda5710f62c757522 (MD5) Previous issue date: 2006
The anti-inflammatory pentacyclic triterpene, oleanolic acid (OA) was examined on acute nociception induced by intraplantar injection of capsaicin in mice. OA administered orally to mice at 10, 30 and 100 mg kg−1, significantly attenuated the paw-licking response to capsaicin (1.6 μg/paw) by 53%, 68.5% and 36.6%, respectively. Ruthenium red (3 mg kg−1, s.c.), a non-competitive vanilloid receptor (V1, TRPV1)-antagonist also suppressed the capsaicin nociception by 38.6%. The maximal antinociception produced by 30 mg kg−1 OA was significantly blocked in animals pre-treated with naloxone (2 mg kg−1, i.p.), the opioid antagonist; l-arginine (600 mg kg−1, i.p.), the substrate for nitric oxide synthase; or glibenclamide (2 mg kg−1, i.p.), the KATP-channel blocker, but was unaffected by yohimbine (2 mg kg−1, i.p.), an α2-adrenoceptor antagonist. In open-field and rota-rod tests that detect motor deficits, mice received 30 mg kg−1 OA did not manifest any effect per se, indicating that the observed antinociception is not a consequence of motor abnormality. These data suggest that OA inhibits capsaicin-evoked acute nociception due to mechanisms possibly involving endogenous opioids, nitric oxide, and KATP-channel opening.
