A Study on the Protective Effects of Polygalae Radix on Neurotoxicity Induced by N-methyl-D-aspartic acid(NMDA)

원지(遠志)가 NMDA로 유발된 선경세포 손상에 미치는 효과

  • Lee, Soo-Bae (Dept. of Herbology, College of Oriental Medicine, Kyungwon University) ;
  • Seong, Nak-Sul (National Crop Experiment Station, RDA) ;
  • Lee, Young-Jong (Dept. of Herbology, College of Oriental Medicine, Kyungwon University)
  • 이수배 (경원대학교 한의과대학 본초학교실) ;
  • 성낙술 (농촌진흥청 작물과학원) ;
  • 이영종 (경원대학교 한의과대학 본초학교실)
  • Published : 2005.06.30

Abstract

Objectives : Polygalae Radix (PR) from Polygalae tenuifolia (Polygalaceae) has been clinically used as a sedative, anti-inflammatory, and anti-bacterial agent. To extend pharmacological effects of PR in the central nervous system (CNS) on the basis of its CNS protective effect, the present study was conducted to identify the effect of PR, whether it shows the neuroprotective action against excitatory neurotoxicity. Methods : To identify the protective effect of PR to excitatory neuro-toxic agent, the present study was focused on the PR effect on cell death, that was caused by applying NMDA to nerve cell, elevation of $(Ca^{2+})_i$, releasement of glutamate, and ROS generation. Result : 1. PR methanol extract, at the concentration range of 0.05 to 5 g/ml, significantly inhibited NMDA (1 mM)-induced neuronal cell death as well as MK-801 (non competitive NMDA antagonist). 2. PR methanol extract $(0.5\;{\mu}g/ml)$ inhibited NMDA (1 mM)-induced elevation of cytosolic calcium concentration $[Ca^{2+}]_i$. NMDA application in the presence of MK-801 $(10\;{\mu}M)$ failed to produce the increase of $[Ca^{2+}]_i$ through all the measurement time. 3. PR methanol extract $(0.5\;{\mu}g/ml)$ inhibited the NMDA-induced elevation of glutamate release. Also, MK-801 showed similar protective effects. 4. PR methanol extract $(0.5\;{\mu}g/ml)$ inhibited the NMDA-induced elevation of ROS generation. Also, MK-801 showed similar protective effects. Conclusion : The present study provides the availability of PR to exert its protective effect on the neuronal cell death in various neurodegenerative pathophysiological conditions.

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