Vitis amurensis, Aralia cordata, and Glycyrrhizae radix have been widely used as oriental medicinal plants in Korea, China and Japan and found to possess anti-oxidative and anti-inflammatory activities. A previous study demonstrated a protection of an ethanol extract (SSB) of a mixture of three medicinal plants of Vitis amurensis, Aralia cordata, and Glycyrrhizae radix against β amyloid protein-induced memory impairment. The current study was conducted to investigate the neuroprotective effect of SSB against ischemiainduced brain injury. Transient focal cerebral ischemia was induced by 2 hr middle cerebral artery occlusion followed by 24 hr reperfusion (MCAO/reperfusion) in rats. Oral administration of SSB (5, 10 and 25 mg/kg) 30 min before and 1 h after MCAO, and 1 h after reperfusion reduced MCAO/ reperfusion-induced brain infarct and edema formation. SSB also inhibited development of behavioral disabilities in MCAO/reperfusion-treated rats. Exposure of cultured cortical neurons to 500 μM glutamate for 12 hr resulted in neuronal cell death. SSB (1-10 μg/mL) inhibited glutamateinduced neuronal death, elevation of intracellular calcium concentration ([Ca2+]i), and generation of reactive oxygen species (ROS). These results suggest that the neuroprotective effect of SSB against ischemia-induced brain damage might be associated with its anti-excitotoxic activity and that SSB may have a therapeutic role for prevention of neurodegeneration in stroke.

This experimental study was designed to investigate the effects of Chrysanthemi Flos extract (CFE) on the change of cerebral hemodynamics〔regional cerebral blood flow (rCBF) and mean arterial blood pressure(MABP)〕in normal and cerebral ischemic rats, and to determine the mechanism of action of CFE. This study was also designed to investigate whether CFE inhibit lactate dehydrogenase (LDH) activity in neuronal cells and cytokines production in serum of cerebral ischemic rats. The results were as follows ; 1. CFE increased rCBF and increased MABP significantly in a dose-dependent manner. 2. The CFE-induced increase in rCBF was significnatly inhibited by pretreatment with indometh acin(IDN), an inhibitor of cyclooxygenase and methylene blue(MTB), an inhibitor of guanylate cyclase. 3. The CFE-induced increase in MABP was significnatly inhibited by pretreatment with IDN and MTB. 4. CFE 100㎍/㎖ significantly inhibited lactate dehydrogenase(LDH) activity in neuronal cells. 5. rCBF was significantly and stably increased by CFE (1㎎/㎏, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. 6. In serum, by drawing from femoral arterial blood after middle cerebral arterial occlusion (MCAO) 1 hr and reperfusion 1 hr, sample group was significantly decreased IL-1β production compared to that of the control group. 7. In serum, by drawing from femoral arterial blood after MCAO 1 hr and reperfusion 1 hr, sample group was significantly decreased TNF-α production compared to that of the control group. 8. In serum, by drawing from femoral arterial blood after reperfusion 1 hr, sample group significantly increased TGF-β production compared to that of the control group. 9. In serum, by drawing from femoral arterial blood after reperfusion 1 hr, sample group increased IL-10 production compared to that of the control group. These results suggested that the mechanism of CFE was mediated by cyclooxygenase and guanylate cyclase, and CFE had inhibitive effect on the brain damage by inhibited LDH activity, IL-1β and TNF-α production, but accelerated TGF-β production and IL-10 production.thought that CFE should have an anti-ischemic effect on the improvement of cerebral hemodynamics and inhibitive effect on the brain damage.