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Anticonvulsant Effect of Artemisia capillaris Herba in Mice

  • Woo, Tae-Seon (Uimyung Research Institute for Neuroscience, Sahmyook University) ;
  • Yoon, Seo-Young (Uimyung Research Institute for Neuroscience, Sahmyook University) ;
  • Pena, Ike Campomayor Dela (Uimyung Research Institute for Neuroscience, Sahmyook University) ;
  • Choi, Ji-Young (Uimyung Research Institute for Neuroscience, Sahmyook University) ;
  • Lee, Hye-Lim (Uimyung Research Institute for Neuroscience, Sahmyook University) ;
  • Choi, Yoon-Jung (Uimyung Research Institute for Neuroscience, Sahmyook University) ;
  • Lee, Yong-Soo (Department of Pharmacology, College of Pharmacy, Duksung Women's University) ;
  • Ryu, Jong-Hoon (Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University) ;
  • Choi, Jae-Sue (Department of Food Science and Nutrition, College of Fisheries Science, Pukyong National University) ;
  • Cheong, Jae-Hoon (Uimyung Research Institute for Neuroscience, Sahmyook University)
  • Received : 2011.04.30
  • Accepted : 2011.07.19
  • Published : 2011.07.31

Abstract

In the present study, the anticonvulsant effects of Artemisia capillaris Herba (AC) and its major constituent, esculetin (ECT), were tested and the mechanism studied. Locomotion, Myorelaxation, motor coordination and electroshock seizure experiment were conducted in mice. To identify the anticonvulsant mechanism effect of this drug, chemical-induced seizure in mice and the ionic movement in neuroblastoma cells were also observed. The ethanol extract of AC was orally administered to mice 30 min. prior to testing and ECT was intraperitoneally injected. AC and ECT treatment did not change locomotor activities as well as activities on the rota-rod, which indicates that they did not cause a sedative and myorelaxation effect. AC and ECT treatment increased threshold of convulsion induced by electroshock. AC treatment also inhibited convulsion induced by pentylenetetrazole. In the case of strychnine however, only high dose of AC treatment inhibited convulsion. AC and ECT treatment increased the $Cl^-$ influx into the intracellular area in a dose-dependent manner. On the other hand, bicuculline, a GABA antagonist, inhibited the $Cl^-$ influx induced by AC and ECT. These results indicate that ECT induces the anticonvulsive effect of AC extract through the GABAergic neuron.

Keywords

References

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