Efeitos de óleos essenciais de plantas no tempo de sono induzido por cetamina em camundongos

Estudos anteriores mostraram que óleos essenciais voláteis obtidos de plantas potenciam o tempo de sono induzido por pentobarbital e álcool em camundongos. Cetamina é um anestésico muito utilizado em crianças, sendo conhecida por causar uma anestesia dissociativa. Seus efeitos alucinógenos podem ser reduzidos quando administrada em associação a benzodiazepínicos. O objetivo deste estudo foi determinar a influência dos óleos de Psidium guyanensis (Araçá azedo), Psidium pohlianum (Araçá doce), Psidium guajava (Araçá goiaba), Rosmarinus officinalis (Alecrim) e Lippia alba (Cidreira) no tempo de sono induzido por cetamina em camundongos. Os resultados indicam que o tempo de sono induzido por cetamina foi prolongado pelos óleos essenciais de Psidium guyanensis, Psidium pohlianum, Psidium guajava e Lippia Alba mostrando novas possibilidades de associação com a cetamina a fim de prolongar o seu efeito sedativo, proporcionando uma anestesia mais adequada

Biological and Pharmaceutical Bulletin

Texto completo: acesso restrito.p.82-85Many natural terpenoid compounds from plants exhibit antinociceptive property but very few studies have addressed their efficacy in visceral models of nociception. The present study evaluated the antinociceptive potential of oleanolic acid, a pentacyclic triterpene in the mouse model of colonic nociception induced by mustard oil. We further examined the possible participation of opioid, α2-adrenergic, and transient receptor potential vanilloid 1 (TRPV1)-receptors in its mechanism. Mice were pretreated orally with oleanolic acid (3, 10, 30 mg/kg) or vehicle, and the pain-related behavioral responses to intracolonic injection of mustard oil was analysed. Oleanolic acid significantly suppressed the mustard oil-induced nociceptive behaviors at test doses of 10 and 30 mg/kg, in a dose-related manner. The antinociceptive effect of oleanolic acid (30 mg/kg) was significantly blocked by pretreatment with the opioid antagonist, naloxone (2 mg/kg, i.p.), while the α2-adrenoceptor antagonist, yohimbine (2 mg/kg, s.c.), had no effect. Pretreatment with ruthenium red (3 mg/kg, s.c.), a non-competitive TRPV1 antagonist alone caused significant inhibition of mustard oil-induced nociception but its co-administration with oleanolic acid produced neither antagonism nor potentiation of oleanolic acid antinociception. In the open-field test that detects sedative or motor abnormality, mice received 30 mg/kg oleanolic acid did not show any per se influence, but significantly inhibited the mustard oil-induced decrease in ambulation frequency. These data demonstrate the visceral antinociceptive potential of oleanolic acid that involves an opioid mechanism and possibly a modulatory influence on vanilloid-receptors, which needs further study

Pharmacological Research

RESTRITOThe 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