Comparative anticonvulsant activities of the essential oils (EOs) from Cymbopogon winterianus Jowitt and Cymbopogon citratus (DC) Stapf. in mice

Monalisa Ribeiro Silva, Rafael Matos Ximenes, José Galberto Martins da Costa, L. Kalyne A. M. Leal, Amanda A. de Lopes, Glauce Socorro de Barros Viana

The fresh leaves of Cymbopogon citratus are a good source of an essential oil (EO) rich in citral, and its tea is largely used in the Brazilian folk medicine as a sedative. A similar source of EO is Cymbopogon winterianus, rich in citronellal. The literature presents more studies on the EO of C. citratus and their isolated bioactive components, but only a few are found on the EO of C. winterianus. The objective of the present study was then to study, in a comparative way, the effects of both EOs on three models of convulsions (pentylenetetrazol, pilocarpine, and strychnine) and on the barbiturate-induced sleeping time on male Swiss mice. The animals (20-30 g) were acutely treated with 50, 100, and 200 mg kg(-1), intraperitoneally, of each EO, and 30 min later, the test was initiated. The observed parameters were: latency to the first convulsion and latency to death in seconds. Furthermore, the in vitro effects of the EOs were also studied on myeloperoxidase (MPO; a biomarker for inflammation) and lactate dehydrogenase (LDH; an index of cytotoxicity) releases from human neutrophils. The EOs radical-scavenging activities were also evaluated by the 1,1-diphenyl-2-picrylhydrazyl (DPPH) assay. The results showed that both EOs were more active on the pentylenetetrazol-induced convulsion model, and C. citratus was even more efficient in increasing latency to the first convulsion and latency to death. Both parameters were potentiated in the presence of a lower dose of diazepam (reference drug) when associated to a lower dose of each EO (25 mg kg(-1)). Besides, their anticonvulsant effects were blocked by flumazenil, a known benzodiazepine antagonist. This effect was somewhat lower on the pilocarpine-induced convulsion, and better effects were seen only with the EOs' higher doses (200 mg kg(-1)). A similar result was observed on the strychnine-induced convulsion model. Both EOs potentiated the barbiturate-induced sleeping time. However, C. citratus was more efficient. Interestingly, both EOs completely blocked the MPO release from human neutrophils and showed no cytotoxic effect on the LDH release from human neutrophils. On the other hand, only a very low or no effect on the DPPH assay was observed with C. winterianus and C. citratus, respectively, indicating that the radical scavenging activity did not play a role on the EOs' effects. We conclude that the mechanism of action of the anticonvulsant effect of the EOs studied is, at least in part, dependent upon the GABAergic neurotransmission. In addition, their effects on inflammatory biomarkers can also contribute to their central nervous system activity.