Effect of Chengsimyeunja-eum (淸心蓮子飮) and Sunghyangjungi-san (星香正氣散) on Streptozotocin-induced Ischemic Damaged Diabetic Rats

청심연자음(淸心蓮子飮)과 성향정기산(星香正氣散)이 Streptozotocin유발(誘發) 당뇨(糖尿)흰쥐의 뇌허혈 손상(腦虛血 損傷)에 미치는 영향(影響)

  • Park, Soon-Il (Effect of Chengsimyeunja-eum (淸心蓮子飮) and Sunghyangjungi-san (星香正氣散) on Streptozotocin-induced Ischemic Damaged Diabetic Rats) ;
  • Lee, Won-Chul (Dept. of Oriental Medicine, Graduate School, Dongguk University)
  • 박순일 (동국대학교 한의과대학 내과학교실) ;
  • 이원철 (동국대학교 한의과대학 내과학교실)
  • Published : 2007.09.30

Abstract

Objectives : Chengsimyeunja-eum and Sunghyangjungi-san are prescriptions used for cerebral infarction clinically; it is known that these formulas reduce ischemic damage. According to previous research data, controlling certain types of glucose is considered to decrease the risk of cerebral infarction. Based on this fact, we investigated the effects of Chengsimyeunja-eum and Sunghyangjungi-san extracts on reperfusion following ischemic damage to diabetic rats, the change of c-FOS and Bax positive neurons in the hippocampus and cerebral cortex and protein through immunohistochemical methods, changes of serum glucose level, serum triglyceride level, and hepatic glucokinase activity. Methods : We induced ischemic damaged in diabetic rats, and the rats were administered Chengsimyeunja-eum and Sunghyangjungi-san extracts. Results : Chengsimyeunja-eum demonstrated significant decrease of c-Fos positive neurons in both hippocampus and cerebral cortex as well as a significant decrease of Bax positive neurons in hippocampus after ischemic damage on diabetic rats and decrease of serum glucose level after ischemic damage on diabetic rats. Sunghyangjungi-san demonstrated significant decreases of c-Fos and Bax positive neurons in both hippocampus and cerebral cortex after ischemic damage on diabetic rats. Conclusions : Chengsimyeunja-eum, effect on glucose level control, has a remarkable effect of protection of neurons not effective on glucose level. Sunghyangjungi-san showed neuroprotective effect through preventing neuronal cell death.

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