title: Inhibitory role of Acorus calamus in ferric chloride-induced epileptogenesis in rat.
abstract: The roots and rhizomes of Acorus calamus (Family: Araceae) have been used in the ancient systems of medicine for the treatment of various neurological disorders. Of the various methods used for inducing experimental epileptic models, the intracortical administration of ferric chloride (FeCl(3)) into sensorimotor cortex induces recurrent seizures and epileptic discharge similar to human post-traumatic epilepsy through the generation of free radicals. The present study focuses on the effect of Acorus calamus on the behavioral, electroencephalographic, and antioxidant changes in FeCl(3)-induced rat epileptogenesis. Topical administration of FeCl(3) (5 microL; 100 mM) into the sensorimotor cortex of rats showed an increase in the wet dog shake behavior, spike wave discharges together with an significant increase in antioxidant enzyme activity, such as superoxide dismutase and catalase, resulting in an increase in the level of lipid peroxidation in cerebral cortex. Pretreatment with Acorus calamus (200 mg/kg b.w., p.o. for 14 days) and also diazepam (DZ, 20 mg/kg b.w., i.p.) decreased the WDS behavior, spike wave discharges with single isolated positive waves, and a significant decrease in activity of superoxide dismutase and level of lipid peroxidation was observed in cerebral cortex with respect to those observed in FeCl(3)-induced epileptic group. Data presented in this study clearly show that Acorus calamus possesses the ability for preventing the development of FeCl(3)-induced epileptogenesis by modulating antioxidant enzymes, which in turn exhibit the potentiality of Acorus calamus to be developed as an effective anti-epileptic drug.
authors: S. N. Pradhan Centre for Neurosciences, University of Calcutta, Kolkata, India. rhazra@emory.edu
authors: R
authors: R
authors: Hazra
authors: K
authors: K
authors: Ray
authors: D
authors: D
authors: Guha
mesh_terms: D029023:Acorus / Q000737:chemistry*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D002712:Chlorides; D004195:Disease Models, Animal; D004569:Electroencephalography; D004827:Epilepsy / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D005290:Ferric Compounds / Q000037:antagonists & inhibitors / Q000633:toxicity; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D009676:Noxae / Q000037:antagonists & inhibitors / Q000633:toxicity; D010936:Plant Extracts / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D027343:Rhizome / Q000737:chemistry; D013003:Somatosensory Cortex / Q000187:drug effects / Q000201:enzymology / Q000503:physiopathology; D013482:Superoxide Dismutase / Q000378:metabolism; D014202:Tremor / Q000139:chemically induced / Q000517:prevention & control
chemical_list: D002712:Chlorides; D005290:Ferric Compounds; D018696:Neuroprotective Agents; D009676:Noxae; D010936:Plant Extracts; D002374:Catalase; D013482:Superoxide Dismutase; C024555:ferric chloride