Anticonvulsant Activity of Methanolic Extract of Acorus Calamus Leaves in Albino Mice

Pharmaceutical Sciences-Pharmacology for drug discovery

Abstract

Acorus calamus, commonly known as sweet flag, has a long history of use in the treatment of a variety of ailments
including inflammation, chest pain, digestive disorders and some mental illnesses. Its effects on the neurological conditions have
been well documented for axinolytic and antidepressant activities. With this background, the aim of the present study is evaluate
the anticonvulsant activity of methanolic extract of Acorus calamus leaves in albino mice. The study included albino mice divided
into 8 groups of 6 mice each. Maximum electroshock induced seizures (MES) and Pentylenetetrazole (PTZ) tests were
performed on the animal models to evaluate the antiepileptic activity (4 groups were allocated to MES and 4 to PTZ). The
methanolic extract of Acorus calamus leaves exhibited a significant reduction in the duration of hind limb extensor phase in MES
model (7.116±0.501 seconds for control and 9.116± 0.527 seconds for extract) and delayed the latency of seizures induced by
PTZ (485.500±14.941 seconds) when compared with that of the control group (297.000±21.918 seconds). In addition, the
groups administered with the extract and sodium valproate in combination exhibited significant results in both MES and PTZ
models (T2- 92.61% and T4- 21.95 %, respectively). Preliminary phytochemical screening performed in several studies has shown
the presence of triterpenoids, flavonoids, saponins and tannins. The anticonvulsant activity of Acorus calamus may be mediated by
its GABA potentiating activity. It can thus be concluded that the observed anticonvulsant effects could be the resultant of a
synergistic action of these phytochemicals. Further studies should be undertaken to substantiate these results on various animal
models along with a thorough phytochemical analysis and in silico studies to understand the mode of action of these
phytochemicals on various GABA receptor-mediated signaling.