• Proceedings of the Plant Resources Society of Korea Conference
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• 2021.04a
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• pp.57-57
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• 2021

Oxygen glucose deprivation/re-oxygenation (OGD/R) induces neuronal injury via mechanisms that are believed to mimic the pathways associated with brain ischemia. Stachys sieboldii Miq. (Chinese artichoke), which has been extensively used in oriental traditional medicine to treat of ischemic stroke; however, the role of S. sieboldii Miq. (SSM) in OGD/R induced neuronal injury is not yet fully understood. The present research is aimed to investigate the protective effect and possible mechanisms of SSM extract treatment in an in vitro model of OGD/R to simulate ischemia/reperfusion Injury. Pretreatment of these cells with SSM significantly attenuated OGD/R-induced production of reactive oxygen species (ROS) by increasing GPx, SOD, and decreasing MDA. SSM decreased mitochondrial damage caused by OGD/R injury and inhibited the release of cyt-c from mitochondrion to cytoplasm in SH-SY5Y cells. Furthermore, neuronal cell apoptosis caused by OGD/R injury was inhibited by SSM, and SSM could decrease apoptosis by increasing ratio of Bcl-2/Bax and inhibiting caspase signaling pathway in SH-SY5Y cells. SSM demonstrated a neuroprotective effect on the simulated cerebral ischemia in vitro model, and this effect was the inhibition of mitochondria-mediated apoptosis pathway by scavenging of ROS generation. Therefore, SSM may be a promising neuroprotective strategy against ischemic stroke.

• BMB Reports
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• v.50 no.11
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• pp.590-595
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• 2017

High-mobility group box-1 (HMGB-1) is expressed in almost all cells, and its dysregulated expression correlates with inflammatory diseases, ischemia, and cancer. Some of these conditions accompany HMGB-1-mediated abnormal angiogenesis. Thus far, the mechanism of HMGB-1-induced angiogenesis remains largely unknown. In this study, we performed time-dependent DNA microarray analysis of endothelial cells (ECs) after HMGB-1 or VEGF treatment. The pathway analysis of each gene set upregulated by HMGB-1 or VEGF showed that most HMGB-1-induced angiogenic pathways were also activated by VEGF, although the activation time and gene sets belonging to the pathways differed. In addition, HMGB-1 upregulated some VEGFR signaling-related angiogenic factors including EGR1 and, importantly, novel angiogenic factors, such as ABL2, CEACAM1, KIT, and VIPR1, which are reported to independently promote angiogenesis under physiological and pathological conditions. Our findings suggest that HMGB-1 independently induces angiogenesis by activating HMGB-1-specific angiogenic factors and also functions as an accelerator for VEGF-mediated conventional angiogenesis.

• Clinical and Experimental Pediatrics
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• v.61 no.8
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• pp.245-252
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• 2018

Purpose: This study investigated patterns of ischemic injury observed in brain images from patients with neonatal group B Streptococcal (GBS) meningitis. Methods: Clinical findings and brain images from eight term or near-term newborn infants with GBS meningitis were reviewed. Results: GBS meningitis was confirmed in all 8 infants via cerebrospinal fluid (CSF) analysis, and patients tested positive for GBS in both blood and CSF cultures. Six infants (75.0%) showed early onset manifestation of the disease (<7 days); the remaining 2 (25.0%) showed late onset manifestation. In 6 infants (75%), cranial ultrasonography showed focal or diffuse echogenicity, suggesting hypoxic-ischemic injury in the basal ganglia, cerebral hemispheres, and periventricular or subcortical white matter; these findings are compatible with meningitis. Findings from magnetic resonance imaging (MRI) were compatible with bacterial meningitis, showing prominent leptomeningeal enhancement, a widening echogenic interhemisphere, and ventricular wall thickening in all infants. Restrictive ischemic lesions observed through diffusion-weighted imaging were evident in all eight infants. Patterns of ischemic injury as detected through MRI were subdivided into 3 groups: 3 infants (37.5%) predominantly showed multiple punctuate lesions in the basal ganglia, 2 infants (25.0%) showed focal or diffuse cerebral infarcts, and 3 infants (37.5%) predominantly showed focal subcortical or periventricular white matter lesions. Four infants (50%) showed significant developmental delay or cerebral palsy. Conclusion: Certain patterns of ischemic injury are commonly recognized in brain images from patients with neonatal GBS meningitis, and this ischemic complication may modify disease processes and contribute to poor neurologic outcomes.

• Journal of Veterinary Clinics
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• v.31 no.5
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• pp.457-460
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• 2014

This case study describes the magnetic resonance characteristics of brain infarction in three dogs. Locations of the brain infarcts were cerebella, thalamus, and multifocal. The infarcts were sharply demarcated from adjacent brain parenchyma, homogeneous, T1-hypointense, T2-hyperintense with/without contrast enhancement, and minimal or no mass effect. Diffusion-weighted imaging (DWI) sequences were available in a dog and the infarcts were hyperintense on DWI and were hypointense on the apparent diffusion coefficient map.

• Journal of Korean Biological Nursing Science
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• v.4 no.2
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• pp.19-40
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• 2002

The purpose of this study was to determine the effect of DHEA on Type I(soleus) and II muscles(plantaris, gastrocnemius) in a focal brain ischemia model rat. Thirty-seven male Sprague-Dawley rats with $200{\sim}250g$ body weights were randomly divided into four groups : CINS(cerebral ischemia + normal saline), CIDH(cerebral ischemia + DHEA), SHNS(sham + normal saline), SHDH (sham + DHEA). Both the CINS and CIDH groups were undergone a transient right middle cerebral artery occlusion operation. In the SHNS and SHDH groups, a sham operation was done. DHEA was administered daily at a dose of 0.34mmol/kg, and normal saline was administered daily at the same dose by intraperitoneal injection for 7days after operation. Cerebral infarction in the CINS and CIDH groups was identified by staining with 2% triphenyltetrazolium chloride solution for 60 minutes. The data were analyzed by Kruskal-Wallis test and Mann-Whitney U test using the SPSSWIN 9.0 program. The results were summarized as follows: 1) The muscle weights of soleus(Type I), plantaris and gastrocnemius(Type II) in CINS group were significantly less than those of the SHNS group(p<.01). The muscle fiber cross-sectional area of the CINS group was significantly less than that of the SHNS group in Type I muscle fiber of the soleus and Type II muscle fiber of the plantaris and gastrocnemius(p<.05). The myofibrillar protein content of the CINS group was significantly less than that of the SHNS group in the left gastrocnemius and right soleus(p<.05). 2) The muscle weights of the soleus, plantaris and gastrocnemius except the unaffected side of the plantaris in the CIDH significantly increased compared to those of the CINS group(p<.05). The muscle fiber cross-sectional area of the CIDH group significantly increased compared to that of the CINS group in Type II muscle fiber of the plantaris and gastrocnemius(p<.05). The myofibrillar protein content of the CIDH group significantly increased compared to that of the CINS group in the left soleus(p<.05). 3) On the post-op 8 day, the body weight of the CINS group was significantly less than that of the CIDH, SHNS and SHDH groups(p<.01). Total diet intake of the CINS and CIDH groups was significantly less than that of the SHNS and SHDH groups(p<.01). Based on these results, it was identified that muscle atrophy could be induced during the 7 days after cerebral infarction, and DHEA administration during the early stage of cerebral infarction might attenuate muscle atrophy.

• The Journal of Dong Guk Oriental Medicine
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• v.8 no.1
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• pp.107-116
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• 1999

The effects of Sosokmyung-tang(小續命湯) on global cerebral ischemia and cerebral in farction by MCA(middle cerebral artery) occlusion were evaluated in this study. This study was performed to investigate that Sosokmyung-tang would be useful for cerebrovascular diseases. In the case of global cerebral ischemia, ICR mice were used and divided into three group at random. Control group was treated after oral administration of normal saline, experimental group was treated after oral administration of 10.4mg/20g/day of Sosokmyung-tang extract. The multiple parameter of global cerebral ischemia included the duration of coma of KCN(potassium cyanide)-injected(1.2mg/kg, i.v) group and the survival time of KCN-injected(3.0mg/kg, i.v) group. In the case of cerebral infarction by MCA occlusion, Sprague-Dawley rats were used and divided into three group at random. Control group was given nothing before MCA occlusion, experimental group was given 157.2mg/250g/day of Sosokrnyung-tang extract before MCA occlusion. We investigated edema and ischemic ratio in 8 slices of rats' brain after MCA occlusion. The results were obtained as follows : 1. Sosokrnyung-tang significantly shortened the duration of coma of KCN-injected(1.2mg/kg,i.v) group and lengthened the survival time of KCN-injected(3.0mg/kg, i.v) group. 2. Sosokmyung-tang significantly decreased cerebral edema and ischemic ratio in rats after MCA occlusion. From the above results, it was concluded that Sosokmyung-tang can be effectively applied to cerebrovascular diseases.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.5
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• pp.475-485
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• 2017

The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7-36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7-36) (10, 20, $40{\mu}g/kg$ i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7-36) at the same dose and route for three times each day. After 72 h, hypoglycemic effects were assessed by blood glucose changes, and neuroprotective effects were evaluated by neurological deficits, infarct volume and histomorphology. Mechanisms were investigated by detecting the distribution and expression of the nuclear factor erythroid-derived factor 2 related factor 2 (Nrf2) in ischemic brain tissue, the levels of phospho-PI3 kinase (PI3K)/PI3K ratio and heme-oxygenase-1 (HO-l), as well as the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA). Our results showed that rhGLP-1 (7-36) significantly reduced blood glucose and infarction volume, alleviated neurological deficits, enhanced the density of surviving neurons and vascular proliferation. The nuclear positive cells ratio and expression of Nrf2, the levels of P-PI3K/PI3K ratio and HO-l increased, the activities of SOD increased and the contents of MDA decreased. The current results indicated the protective effect of rhGLP-1 (7-36) in diabetic rats following MCAO/R that may be concerned with reducing blood glucose, up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD.

• BMB Reports
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• v.53 no.11
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• pp.582-587
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• 2020

It is well known that oxidative stress participates in neuronal cell death caused production of reactive oxygen species (ROS). The increased ROS is a major contributor to the development of ischemic injury. Indoleamine 2,3-dioxygenase 1 (IDO-1) is involved in the kynurenine pathway in tryptophan metabolism and plays a role as an anti-oxidant. However, whether IDO-1 would inhibit hippocampal cell death is poorly known. Therefore, we explored the effects of cell permeable Tat-IDO-1 protein against oxidative stress-induced HT-22 cells and in a cerebral ischemia/reperfusion injury model. Transduced Tat-IDO-1 reduced cell death, ROS production, and DNA fragmentation and inhibited mitogen-activated protein kinases (MAPKs) activation in H₂O₂ exposed HT-22 cells. In the cerebral ischemia/reperfusion injury model, Tat-IDO-1 transduced into the brain and passing by means of the blood-brain barrier (BBB) significantly prevented hippocampal neuronal cell death. These results suggest that Tat-IDO-1 may present an alternative strategy to improve from the ischemic injury.

• The Journal of Internal Korean Medicine
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• v.21 no.1
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• pp.116-125
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• 2000

Objectives : The aim of this study is to investigate that Sunghyangjeongki-San which has been frequently medicated in the early stage of stroke can protect against ischemic damage in rat brain Methods : Extracellular levels of amino acids(glutamate, aspartate, GABA, glycine, taurine, tyrosine, alanine), organic acids(pyruvate, lactate), and cerebral infarction volume were measured at the striatum of rats subjected to permanant focal cerebral ischemia induced by 2 hours of middle cerebral artery occiusion(MCAO). Rats were orally administered with Sunghyangjeongki-San at 30mins before MCAO and the microdialysate was collected by intracerebral microdialysis three times before MCAO and six times after MCAO at 20mins interval and analyzed by HPLC. After a microdialysis study, the brain was sliced and stained with cresyl violet buffer for the measurement of cerebral infarcted area and volume by image analyzer system Results : The concentrations of glutamate, aspartate, and tyrosine known as excitatory neurotransmitters were significantly decreased in Sunghyangjeongki-San group compared with control group, The concentrations of GABA, glycine, taurine and alanine known as inhibitory neurotransmitters were significantly increased in Sunghyangjeongki-San group compared with control group. The concentrations of pyruvate and lactate showed little significant change in Sunghyangjeongki-San group compared with control group. The measurement of cerebral infarcted area and volume by image analyzer system were significantly decreased in Sunghyangjeongki-San group compared with control group. Conclusions : Sunghyangjeongki-San can affect on protecting against cerebral ischemia by regulating extracellular levels of excitatory and inhibitory amino acid neurotransmitters and improve the conditions of the patients in the early stage of stroke.

• Journal of Oriental Neuropsychiatry
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• v.21 no.1
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• pp.59-69
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• 2010

Objectives: The study aims to look into how the application of EA(Electro-acupuncture) in the initial step of ischemic brain injury affects the changes in Bax and Caspase-3 expression among forebrain apoptosis. Methods: It caused GI by using common carotid artery occlusion and conducted the test by dividing into the no applied EA group after 6 hours and 12 hours, the LI 4 EA group that applied EA to LI4, and GV 20 EA group that was applied to GV 20. After that, the following results were obtained by comparing Bax and Caspase-3 expression, which were apoptosis-related factors, with its application time through immunohistochemical staining after extracting brain of each group. Results: According to each group's Bax expression by the application time, the order of expression increase after 6 hours is shown to be the no applied EA group, LI 4 group, and GV 20 group. The stimulation after 12 hours was most lowly expressed in the GV 20 group, and the no applied EA group and LI 4 group showed similar level. Conclusions: EA stimulation in the initial step after ischemia seems to affect positively Bax and Caspase-3 expression that are index of forebrain apoptosis.