• The Journal of Korean Medicine
• /
• v.28 no.3 s.71
• /
• pp.216-231
• /
• 2007

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.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.27 no.2
• /
• pp.173-182
• /
• 2013

This Study was designed to investigate the effects of Sibjeondaebo-tang (SDT) and Gamy-Sibjeondaebo-tang (GST, Sibjeondaebo-tang adding Cervi Pantotrichum Cornu) on the improvement in regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) in normal rats, and in the rats with cerebral ischemia induced by middle cerebral artery occlusion, and further to determine the mechanisms. And, It was to investigate the effects of the SDT and GST with the change of histologic examination through the BDNF in the hippocampus CA1. In changes of cerebral hemodynamics, SDT and GST significantly increased rCBF in a dose-dependent manner but decreased MABP in normal rats. In mechanism of cerebral hemodynamics, Increase of GST-induced rCBF was significantly inhibited by pretreatment with methylene blue (0.01 mg/kg, i.p.), an inhibitor of guanylate cyclase, and Decrease of GST-induced MABP was significantly increased by pretreatment with methylene. These results suggested that the action of GST was mediated by guantlate cyclase pathway. In cerebral ischemics, the rCBF was stably improved by SDT (10 mg/kg, i.p.) significantly and stably increased by GST (10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrast with the findings of rapid and marked increase in Control group. These results suggested that GST had anti-ischemic action in cerebral ischemic state. In histological examination through TTC stain, Sample A group and Sample B group decreased discoloration in the cortical part at $28^{th}$ day after MCAO induction. In immunohistochemistric response of BDNF, Sample A group and Sample B group increased respondent effect at $28^{th}$ day after MCAO induction. These results suggest that GST can Increase rCBF in normal state, as well as improve the stability of rCBF in cerebral ischemic state. Furthermore, methylene blue inhibitor study suggested the mechanism of blood flow enhancement by GST may be mediated by guanylate cyclase pathway.

• Journal of Chest Surgery
• /
• v.35 no.10
• /
• pp.740-744
• /
• 2002

Retrograde cerebral perfusion under hypothermic circulatory arrest is a simple and useful adjunct to avoid cerebral ischemic injury in the treatment of aortic arch pathology. In the surgery of distal aortic arch and proximal descending aortic lesions through the left thoracotomy incision, right atrium-retrograde cerebral perfusion (RA-RCP) through a venous cannula positioned into the right atrium is simpler than retrograde cerebral perfusion through superior vena cava. The time limits for RA-RCP during aortic arch reconstruction have yet to be clarified. We, herein, present a case with uneventful recovery after RA-RCP of 94 minutes during reconstruction of aortic arch and descending aorta. These data suggest that RA-RCP, as an adjunct to hypothermic circulatory arrest, may prolong the circulatory arrest time and thus prevent ischemic injury of the brain, even when RA-RCP exceeds 90 minutes.

• The Korean Journal of Pain
• /
• v.21 no.1
• /
• pp.33-37
• /
• 2008

Background: Cerebral blood vessels are innervated by sympathetic nerves from the superior cervical ganglion (SCG). The purpose of the present study was to evaluate the neuroprotective effect of superior cervical sympathetic ganglion block in rats subjected to permanent focal cerebral ischemia. Methods: Thirty male Sprague-Dawley rats (270-320 g) were randomly assigned to one of three groups (control, lidocaine and ropivacaine). A brain injury was induced in all rats by middle cerebral artery occlusion with a nylon thread. The animals of the local anesthetic group received $30{\mu}l$ of 2% lidocaine or 0.75% ropivacaine in the SCG. Neurologic scores were assessed 24 hours after brain injury. Brain samples were then collected. The infarct and edema ratios were measured by 2.3.5-triphenyltetrazolium chloride staining. Results: There were no differences in the death rates, neurologic scores, or infarction and edema ratios between the three groups. Conclusions: These findings suggest that superior cervical sympathetic ganglion block may not influence the brain damage induced by permanent focal cerebral ischemia in rats.

• The Journal of Internal Korean Medicine
• /
• v.25 no.3
• /
• pp.473-481
• /
• 2004

Objective : In this study old BCAO rats were observed for effects of 'Dea-Hwang' on brain ischema injury, because risk of stroke increases with age. Method : The brain ischema injury was induced by temporarily closing carotids on both sides in a low blood pressuer state and Dea-Hwang was administered orally to 18 month-old BCAO rats. Results and Conclusions : The ischemically damaged Hippocampus and c-fos and c-jun expression were analyzed by immunohistochemical staining and results are summarized as follows: 1. The c-fos expression after inducing a brain ischema injury in the hippocampus was more inhibited in the dosed group than in the control group. 2. The normalized optical density of c-fos expression was more reduced in the CA1, CA2, and DG areas of the dosed group than in those of the control group. 3. The c-jun expression after inducing brain ischema injury in the hippocampus was more inhibited in the dosed group than in the control group. 4. The normalized optical density of c-jun expression was more reduced in the CAI area of the dosed group than in that of the control group.

• Korean Journal of Pharmacognosy
• /
• v.34 no.4 s.135
• /
• pp.335-338
• /
• 2003

It is thought that highly reactive oxygen species generated after strokes plays a key role in damaging the brain. We examined free radical scavenging activity and neuroprotective effects of several medicinal herbs in a rat model of transient ischemia. Free radical scavenging property of medicinal herbs was examined in vitro using 1,1-diphenyl-2-picrylhydrazyl stable free radical. Transient ischemia was induced by intraluminal occlusion of the right middle cerebral artery for 120 min, followed by reperfusion for 22 hr in rats. Aqueous extracts of 8 medicinal herbs (200 mg/kg) were orally administered twice to transient ischemic rat prior to reperfusion and 2 hr after reperfusion. Total infarction volume in the hemisphere ipsilateral to the ischemia-reperfusion was significantly decreased in 7 groups treated with Sophora flavescens, Lycopus lucidus, Sanguisorba officinalis, Caesalpinia sappan, Albizia julibrissin, Rubia akane, Psoralea corylifolia, or Prunella vulgaris. However, neuroprotective effects of these medicinal herbs were not correlated with their antioxidative activities. These results suggest that these medicinal herbs exert neuroprotection via antioxidative as well as unknown mechanism.

• KOREAN JOURNAL OF CROP SCIENCE
• /
• v.50 no.spc1
• /
• pp.220-223
• /
• 2005

As functional evaluation of mulberry fruits extracts, the protective effect on cerebral cell and antibacterial activities were carried. $1\%$ HCl-MeOH extract showed $37\%$ cytoprotective effect on hydrogen peroxide, also C3G identified mulberry fruits and cyanidin showed $52\%,\;76\%$, respectively, protective effects on oxygen-glucose deprivation (OGD). In the antibacterial activity of mulberry fruit extracts, MeOB-Cheongil extract showed the highest inhibitory activity. Salmonella typhimurium was shown inhibitory rate more than $70\%$ in all treatment groups. Also Klebsiella pneumoniae was shown inhibitory activity in all treatment groups.

• The Journal of Korean Medicine
• /
• v.25 no.3
• /
• pp.32-44
• /
• 2004

Objectives : This study was undertaken to prove the effect of GSHT on the glutamate receptor, free radical and brain damage in rats subjected to brain ischemia Methods : Levels of cultured cortical neuron death caused by toxic chemicals were measured by LDH release assay. Neuroprotective effects of GSHT on brain tissues were examined in vivo by ischemic model of middle cerebral artery (MCA) occlusion. Results : GSHT showed significant inhibitory effect on LDH release induced by NMDA-kinate-Fe/sup 2+/. GSHT remarkably decreased coma duration time in a nonfatal dose of KCN and showed higher survival rate in a fatal dose. GSHT remarkably decreased ischemic area and edema induced by the MCA blood flow block. GSHT showed high improvement of forelimb and hind limb test after MCA occlusion in neurological examination. GSHT showed no significant change after MCA occlusion in pathological observation of the normal group. Conclusions : These results indicate that GSHT can be used to treat the brain damage caused by brain ischemia. Further study will be needed about the functional mechanism, etc.

• Journal of the Korea Convergence Society
• /
• v.6 no.5
• /
• pp.287-294
• /
• 2015

The purpose of this study, was Let's examine the exposure dose at the time of cerebral blood flow CT scan of acute ischemic stroke patients. In particular, long-term high doses of radiation sensitive organs and we Measured using phantom and a glass dosimeter. Apply the existing protocol suggested by the manufacturer (fixed time delay technique) and the proposed new convergence protocol (bolus tracking technique), reporting to measure the dose, dose reduction was to prepare the way. Results up to 39.8% as compared to the existing protocols in a new suggested convergence protocol, a minimum of 5.8% was long-term dose is reduced. Test dose of $CDTI_{vol}$ and DLP values decreased 25%, respectively, were measured at less than recommended dose. Try checking the protocol set out in the existing based on the analysis result of the above, by applying the proposed new convergence protocol by reducing the dose would have to contribute to improved public health. It is believed to be research continues to find the optimum protocol in the other tests.

• The Journal of Internal Korean Medicine
• /
• v.24 no.1
• /
• pp.11-20
• /
• 2003

Objective : Experimental studies have been done to elucidate the effect of kangwhalyupung-tang(KWYPT) on neuronal cell damage induced by brain ischemia. Method : The cytotoxic effect of ischemia was measured in the MTS assay cultures. MTS assay, INT assay, neurofilament(NF) enzymeimmuno assay(EIA). And the KWYPT on ischemia-induced neurotoxicity were examined by in vitro assays. Results : 1. The KWYPT protected effectively neuronal cell-death resulted from brain ischemia induced by the treatment of $95%N_2/5%CO_2$ for 10 min in those dependent fashion. 2. The KWYPT effectively increased the amount of NF resulting from brain ischemia, induced by the treatment of $95%N_2/5%CO_2$ for 15 min in those dependent fashions. Conclusions : KWYPT protects the brain ischemia-induced neurotoxicity through the increase of cell viability and of neurofilament in dose-dependent manner.