• Journal of Korean Academy of Nursing
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• v.34 no.1
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• pp.150-159
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• 2004

Purpose: The purpose of this study was to determine the effect of DHEA on hindlimb muscles(soleus, plantaris and gastrocnemius) in a focal brain ischemia model rat. Method: Twenty-seven male Sprague-Dawley rats were randomly divided into three groups: CINS(cerebral ischemia + normal saline), CIDH(cerebral ischemia + DHEA), or SHNS(sham + normal saline). Both the CINS and CIDH groups underwent a transient right middle cerebral artery occlusion operation. In the SHNS group, a sham operation was done. 0.34mmol/kg DHEA was administered daily by an intraperitoneal injection for 7days. Results: The muscle weight, muscle fiber cross-sectional area of the Type I muscle fiber of soleus and Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of gastrocnemius, and muscle strength in the CINS group decreased compared with the SHNS group. The muscle weight, muscle fiber cross-sectional area of the Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of soleus, and muscle strength in the CIDH group increased compared with the CINS group. Conclusion: It was identified that muscle atrophy could be induced during 7 days after a cerebral infarction, and DHEA administration during the early stages of a cerebral infarction might attenuate muscle atrophy.

• Biomolecules & Therapeutics
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• v.25 no.4
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• pp.383-389
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• 2017

Dexmedetomidine is an ${\alpha}2$-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of $1{\mu}g/kg$ load dose, followed by $0.05{\mu}g/kg/min$ infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-$1{\beta}$, interleukin-6 and tumor nevrosis factor-${\alpha}$ as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-${\kappa}Bp65$, inhibitor of ${\kappa}B{\alpha}$ and phosphorylated of ${\kappa}B{\alpha}$ in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-${\kappa}B$ pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.

• The Journal of Korean Medicine
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• v.27 no.2 s.66
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• pp.70-85
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• 2006

Objectives; This study examined the neuroprotective effect of Hyulbuchookautang (血府逐瘀湯, HBCAT)against neural damage following focal cerebral infarction. Methods : Sprague-Dawley Rats were induced with focal cerebral infarction by temporal middle cerebral artery occlusion (MCAO). The rats were divided into 2 groups. We treated extract of HBCAT to one group after operation (sample group), and the other group wasn't treated after operation (control group). We observed neurological scores and TIC-stained infarct area, total infarct volume in brain sections and Bax-positive neurons, HSP70- positive neurons in brain regions. Results : HBCAT treatment at 3 days after MCAO reduced neurological scores induced by MCAO. HBCAT treatment at 5 days after MCAO reduced TTC-stained infarct area in brain sections induced by MCAO. HBCAT treatment at 5 days after MCAO reduced total infarct volume in brain sections induced by MCAO. HBCAT treatment after MCAO reduced Bax-positive neurons in cortex infarct core and cortex infarct penumbra and caudo-putamen of brain regions induced by MCAO. HBCAT treatment after MCAO reduced HSP70- positive neurons in cortex infarct penumbra of brain regions induced by MCAO. Conclusions : These results suggest that HBCAT has a neuroprotective effect against focal cerebral ischemia.

• Journal of Korean Neurosurgical Society
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• v.54 no.1
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• pp.1-7
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• 2013

Objective : This study was undertaken in the belief that the atypical antipsychotic drug quetiapine could prevent apoptosis in the penumbra region following ischemia, taking into account findings that show 5-hydroxytryptamine-2 receptor blockers can prevent apoptosis. Methods : We created 5 groups, each containing 6 animals. Nothing was done on the K-I group used for comparisons with the other groups to make sure adequate ischemia had been achieved. The K-II group was sacrificed on the 1st day after transient focal cerebral ischemia and the K-III group on the 3rd day. The D-I group was administered quetiapine following ischemia and sacrificed on the 1st day while the D-II group was administered quetiapine every day following the ischemia and sacrificed on the 3rd day. The samples were stained with the immunochemical TUNEL method and the number of apoptotic cells were counted. Results : There was a significant difference between the first and third day control groups (K-II/K-III : p=0.004) and this indicates that apoptotic cell death increases with time. This increase was not encountered in the drug groups (D-I/D-II : p=1.00). Statistical analysis of immunohistochemical data revealed that quetiapine decreased the apoptotic cell death that normally increased with time. Conclusion : Quetiapine is already in clinical use and is a safe drug, in contrast to many substances that are used to prevent ischemia and are not normally used clinically. Our results and the literature data indicate that quetiapine could help both as a neuronal protector and to resolve neuropsychiatric problems caused by the ischemia in cerebral ischemia cases.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.303.1-303.1
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• 2002

Recent studies have suggested that the cerebral ischemia induced the neuronal cell death by mediating multiple mechanisms with necrosis and/or apoptosis. The present study examined neuroprotective mechanism of aloesin against transient focal cerebral ischemia. Aloesin. main component of aloe possesses various biological activates such as wound healing. anti-gastric ulcer. and chemopreventive activity. Transient focal cerebral ischemia was induced by 120 min MCAO. (omitted)

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.62-62
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• 2003

It is now convincing that free radical generation is involved in the pathophy siological mechanisms of ischemic stroke, particularly in ischemia-reperfusion injury. The present study, therefore, examined neuroprotective effect of aloesin isolated from Aloe vera, which was known to have antioxidative activity, in a rat model of transient focal cerebral ischemia. Transient focal cerebral ischemia was induced by occlusion of middle cerebral artery for 2 hr with a silicone-coated 4-0 nylon monofilament in male Sprague-Dawley rats under isoflurane anesthesia Aloesin (1, 3, 10, 30 and 50 mg/kg/injection) was administered intravenously 3 times at 0.5, 2 and 4 hr after onset of ischemia. Neurological score was measured 24 hr after onset of ischemia immediately before sacrifice. Seven serial coronal slices of the brain were stained with 2,3,5-triphenyltetrazolium chloride and infarct size was measured using a computerized image analyzer. Treatment with the close of 1 or 50 mg/kg did not significantly reduce infarct volume compared with the saline vehicle-treated control group. However, treatments with the closes of 3 and 10 mg/kg significantly reduced both infarct volume and edema by approximately 47% compared with the control group, producing remarkable behavioral recovery effect. Treatment with the close of 30 mg/kg also significantly reduced infarct volume to a lesser extent by approximately 33% compared with the control group, but produced similar degree of behavioral recovery effect. In addition, general pharmacological studies showed that aloesin was a quite safe compound. The results suggest that aloesin can serve as a lead chemical for the development of neuroprotective agents by providing neuroprotection against focal ischemic neuronal injury.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.04a
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• pp.35-36
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• 1995

To gain insight into the etiological mechanism of dementia and to develop clinically effective congnitive enhancers, it is required to prepare animal models with symptoms and mechanism resemble to that in human. Dementia is mainly classified into two types : senile type of Alzheimer's disease (STAD) and cerebral ischemia-induced one. As animal models of cerebral ischemia, a couple of types in rats have been introduced : one is the occlusion of bilateral carotid arteries-induced forebrain/global ischemia and the other is the occlusion of middle cerebral arteries-induced focal/regional ischemia.

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

• Journal of Korean Biological Nursing Science
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• v.10 no.1
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• pp.1-10
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• 2008

Purpose: The purpose of this study was to investigate the cerebral infarction size, antioxidant enzyme activities and lipid peroxidation changes after 6 weeks of dietary soybean protein intake in a rat focal brain ischemia model. Method: Weaning Sprague-Dawley rats were fed with either modified AIN-93G diet containing casein 20% (control), 20% soybean protein isolate-based diet (S20), or 40% of soybean protein isolate-based diet (S40) for 6 weeks. The animals were subject to right middle cerebral artery occlusion for 2 hr. After 24 hr of recirculation, the rats were sacrificed. Antioxidant enzymes activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and thiobarbituric acid reactive substance (TBARS) level in the right brain were also measured. Result: There were no significant differences in the right cortical infarction volume, TBARS level, SOD and CAT activities among the three groups whereas the GPx activities of the S20 group were significantly higher than those of the control group (p=.02). Conclusion: Our results suggest that 20% of soybean protein may have a modulating effect on GPx and possibly have some protective effect against oxidative stress although it may enough to decrease cerebral infarction volume in rat focal brain ischemia model.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.3
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• pp.741-747
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• 2007

This study evaluated neuroprotective effects of Yanggyuksanhwa-tang (YST), which have been known to be efficacy in the treatment of the stroke and diabetes. on focal cerebral ischemia of diabetic rats. On primary experiment, diabetic condition in rats was induced by streptozotocin injection, then, focal cerebral ischemia was induced by the middle cerebral artery occlusion (MCAO) under the diabetic condition. Then neuroprotective effect of YST was observed with changes of infarct size and volume, expressions of c-Fos, Bax, and hypoxia inducible factor (HIF)-1${\alpha}$ in the brain tissues by using 2% 2,3,5-triphenyltetrazolium chloride (TTC) staining and immunohistochemistry. YST treatment showed a significant decrease of infarct size and volume induced by MCAO in diabetic rats. YST treatment showed a significant decrease of c-Fos and Bax positive neurons in cortex penumbra. YST treatment showed a decrease of HIF-l${\alpha}$ positive neurons in cortex penumbra, but it was not significant statistically. These results suggest that YST has effects on neuroprotection against cerebral infarct under diabetic condition. And it is supposed that neuroprotective effect of YST reveals by anti-apoptosis mechanism.