Protection of spontaneous and glutamate-induced neuronal damages by Soeumin Sibjeundaibo-tang and Soyangin Sibimijihwang-tang in cultured mice cerebrocortical cells

  • Lee, Mi-Young (Department of Oriental Pharmacy, Korea Institute of Oriental Medicine) ;
  • Ma, Jin-Yeul (Department of Oriental Pharmacy, Korea Institute of Oriental Medicine) ;
  • Choo, Young-Kug (Division of Biological Science, College of Natural Sciences, Wonkwang University) ;
  • Jung, Kyu-Yong (Department of Pharmacology, Wonkwang University School of Medicine)
  • Published : 2000.02.29

Abstract

Soeumin Sibjeundaibo-tang (SJDBT) and Soyangin Sibimijihwang-tang (SMJHT) have been used traditionally to improve the systemic blood circulation and biological energy production in the patients with circulatory and neuronal diseases. The object of this study is to determine the protective effects of SJDBT and SMJHT extracts on the spontaneous and glutamate-induced neuronal damages in cultured cells derived from mice cerebral cortex. At 14 days after beginning the cultures, the activity of lactate dehydrogenase released into the culture media was significantly decreased by treatment of cerebroneuronal cells with SJDBT and SMJHT (0.1 mg/ml) for 7 days. By comparison with the normal cells, cerebroneuronal morphology was dramatically changed by treatment of glutamate (1 mM) for 12 hrs, and this was conspicuously recovered by pretreatment of cerebroneural cells with SJDBT and SMJHT (0.1-1.0 mg/ml) for 2 days. Moreover, glutamated-induced DNA fragmentation was also protected by pretreatment of cerebroneuronal cells with those extracts. These results suggest that naturally occurring and glutamate-induced degeneration of cultured cerebrocortical cells may be related, in part, to the process of apoptotic cell death. The pharmacological properties of SJDBT and SMJHT extracts to improve cerebroneuronal degeneration may be considered as one of useful medicines that can prevent cerebrocortical impairments resulted from age-dependent and excitotoxicity-induced neuronal degeneration in human brain.

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