Avaliação dos efeitos farmacológicos de (-)- mentol em modelos comportamentais e de gastroproteção em camundongos

Abstract

Menthol, major constituent of peppermint, has been evaluated in animal models to investigate their activity in the central nervous system through experimental animal models for depression, anxiety, sedation and convulsion, such as forced swimming (FS), tail suspension (TS), open field, elevated plus maze (EPM), rota rod, sleeping time induced by pentobarbital and pentylenetetrazol-induced convulsion. Behavioral effects was also evaluated the role of gastroprotective, seeking to investigate the mechanisms involved, since there is evidence, but few studies on this effect. (-) - Menthol was administered acutely in all tests intraperitoneally at doses of 25 and 50 mg / kg, and in the case of NF, it was also used at a dose of 10 mg / kg. To study the gastroprotective activity, (-)-menthol was administered orally at doses of 100 and 200 mg / kg. The gastric ulcer was induced by administration of 0.2 ml of absolute ethanol or indomethacin (20mg/kg). The results showed that the FS and TS, (-)-menthol showed antidepressant effect at all doses. In the open field test, (-)-menthol increased the number of crossings in doses of 25 and 50 mg / kg, with no significant effect on the dose of 10 mg / kg was not significant. There was increased rearing and decreased grooming. The mechanism of action of anti-immobility menthol seems to be involved with the dopaminergic and noradrenergic systems, perhaps with a possible activation of the dopamine D2 and noradrenergic, likely by activation of adrenergic receptors of type α1. The route rod, at all doses, the motor coordination of animals was not changed. In EPM, (-)-menthol did not change in any parameter. In the sleep time induced by pentobarbital, (-) - menthol reduced the sedative / hypnotic of pentobarbital sodium. Convulsion induced by pentylenetetrazol increased the latency of death. Oral administration of (-)-menthol 100 and 200 mg / kg were able to protect the damage to gastric mucosa by pre-treatment with ethanol and indomethacin. Prior administration of glibenclamide (10 mg / kg, ip) was able to reverse the gastroproteção promoted by (-)-menthol 200 mg / kg in ethanol-induced ulcers. However, pretreatment with L-NAME (10 mg / kg, ip) was not able to reverse gastroprotective effect of (-)-menthol. Measurement of gastric GSH showed that GSH levels increased with the administration of (-)-menthol. In conclusion, this study provides evidence indicating that there is a psychoactive effects of menthol in NC and this seems to be dependent on their interaction with the noradrenergic (α1) and dopamine (D2). Together, these results suggest that menthol has probably stimulating action in the CNS is devoid of anxiolytic and anticonvulsant action is likely. The gastroprotective action promoted by (-)-menthol can be associated with the opening of ATP-dependent K + channels and the increased amount of GSH.