• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.1
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• pp.141-145
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• 2002

In order to clarify the neuroprotective effect of Gamibojungikki-tang (GBJIKT) water extract on cultured mouse spinal sensory neuron damaged by glucose Oxidase (GO), MTT [3-(4,5-dimethylthiazole-2-yl) -2,5-diphenyltetrazolium bromide] assay and SRB (Sulforhodamine B) assay were carried out after the cultured mouse spinal sensory neuron were preincubated with various concentrations of GBJIKT water extract for 3 hours prior to exposure of GO. Cell viability of cultured mouse spinal sensory neurons exposed to various concentrations of GO for 8 hours was decreased in a dose-dependent manner. MTT50 values were 45 mU/ml GO. Cultured mouse spinal sensory neurons in the medium containing various concentration of GO for 8 hours showed decreasing of total protein synthesis. GO was toxic on cultured spinal sensory neurons. Pretreatment at GBJIKT water extract for 3 hours following GO prevented the GO-induced neurotoxicity such as decreasing of total protein synthesis. These results suggest that GO shows toxic effect on cultured spinal sensory neurons and GBJIKT water extract is highly effective in proecting the neurotoxicity induced by GO.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.1
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• pp.190-198
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• 2007

Alzheimer's disease, a representative neurodegenerative disorder, is characterized by the presence of senile plaques and neurofibrillary tangles accompanied by neuronal damages. b-Amyloid peptide is considered to be responsible for the formation of senile plagues that accumulate in the brains of patients with Alzheimer's disease. There has been compelling evidence supporting that b-amyloid-induced cytotoxicity is mediated through generation of reactive oxygen species. In this study, we have investigated the possible protective effect of Rehmannia glutihosaagainst b-amyloid-induced oxidative ceil death in cultured human neuroblastoma SH-SY5Y cells. SH-SY5Y cells treated with b-amyloid underwent apoptotic death as determined by morphological features and positive in situterminal end-labeling (TUNEL staining). Rehmannia glutinosawater extract, wine, and vinegar pretreatments attenuated b-amyloid-induced cytotoxicity and apoptosis. Rehmannia glutinosa vinegar exhibited maximum protective effect by increasing the expression of anti-apoptotic protein, Bcl-2. in addition to oxidative stress, b-amyloid-treatment caused nitrosative stress via marked increase in the levels of nitric oxide, which was effectively blocked by Rehmannia glutinosa. To further explore the possible molecular mechanisms underlying the protective effect of Rehmannia glutinosa, we assessed the mRNA expression of cellular antioxidant enzymes. Treatment of Rehmannia glutinosa vinegar led to up-regulation of heme oxygemase-1 and catalase. These results suggest that Rehmannia glutinosa could modulate oxidative neuronal cell death caused by b-amyloid and may have preventive or therapeutic potential in the management of Alzheimer's disease. Particularly, Rehmannia glutinosa vinegar can augment cellular antioxidant capacity, there by exhibiting higher neuroprotective potential.

• Physical Therapy Rehabilitation Science
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• v.2 no.2
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• pp.87-91
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• 2013

Objective: The present study was aimed at determining the effect of physical training on glutamate transporter activity in a middle cerebral artery occlusion (MCAO)-induced ischemia injury rat model. Design: Randomized controlled trial. Methods: In this study, we randomly divided them into three groups. Group I included non-occlusion sham controls (n=10), Group II included non-physical training after MCAO (n=10), and Group III included rats that were subjected to physical training after MCAO (n=10). Rats in the physical training group underwent treadmill training, which began at 24 h after MCAO and continued for 14 consecutive days. The training intensity was gradually increased from 5 m/min on the first day to 12 m/min on day 3, and it was maintained until day 14. Focal cerebral ischemia was examined in adult male Sprague-Dawley rats by using the MCAO model. We determined the functional outcomes for each rat on days 1, 7, and 14. Glutamate transporter-1 (GLT-1) activity in the cortex of rats from all three groups was examined at the end of the experiment. Results: Out result show that MCAO rats exhibited severe neurological deficits on the 1 day, and there was no statistically significant in each groups. We observed that the functional outcomes were improved at days 7 and 14 after middle cerebral artery occlusion, and GLT-1 activity was increased in the physical training group (p<0.05). Conclusions: These results indicated that physical training after focal cerebral ischemia exerts neuroprotective effects against ischemic brain injury by improving motor performance and increasing the levels of GLT-1 activity.

• KSBB Journal
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• v.27 no.4
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• pp.243-250
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• 2012

The ash content, mineral composition, total phenolics, antioxidant capacity, and neuroprotective effect of the antlers of deer fed with herb-incorporated feedstuff (HFS) or normal feedstuff (NFS) were comparatively evaluated. The contents of ash and mineral of the antler of deer fed with HFS were significantly lower than its counterpart. The ash and mineral contents of deer antlers decreased generally from the upper section toward the tip section. The ratios of Ca/ash, Ca/P, and Ca/Fe of antler of deer fed with HFS were lower than those of antler of deer fed with NFS. Antlers of deer fed with HFS had higher total phenolics, nitrite scavenging capacity, and antioxidant capacity than those of deer fed with NFS. Antlers of deer fed with HFS or NFS showed in vitro neuronal protection of PC-12 cells against oxidative stress in a dose-dependent manner, where antler of deer fed with HFS generally had higher cellular viability than NFS. These results above suggest that the incorporation of the medicinal herbal complex into feedstuff may improve the biological effects of deer antlers.

• Journal of Pharmacopuncture
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• v.22 no.4
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• pp.231-238
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• 2019

Objectives: Alzheimer's disease (AD), an overwhelming neurodegenerative disease, has deleterious effects on the brain that consequently causes memory loss and language impairment. This study was intended to investigate the neuroprotective activity of the two essential oils (EOs) from Iranian Pistacia khinjuk (PK) leaves and Allium sativum (AS) cloves against β-Amyloid 25-35 (Aβ25-35) induced elevation of cholinesterase enzymes in AD. Methods: The EOs of PK (PKEO) and AS (ASEO) were prepared and analyzed in terms of extraction yield, phenolic content, and cholinergic markers in vitro. Moreover, both were administered orally to adult male Wistar rats at concentrations of 1, 2, and 3%. The inhibitory potential of PKEO and ASEO was compared with Donepezil (0.75 mg/kg) against the high activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes. Results: PKEO reached an inhibition rate of 83.6% and 81.4% against AChE and BChE, respectively. ASEO had lower anti-cholinesterase activity (65.4% and 31.5% for the inhibition AChE and BChE). PKEO was found to have more phenolic content than ASEO. A significantly positive correlation was observed between the total phenolics and anti-cholinesterase potential. In rats, both EOs decreased the enzyme activity in a concentration-dependent manner. As compared with Donepezil, the significant difference in the AChE and BChE inhibition occurred as rats were treated with PKEO 3% (p < 0.05). Conclusion: It could be concluded that PKEO and ASEO are potent inhibitors of AChE and BChE in rats that hold promise to be used for the treatment of AD.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.2
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• pp.343-347
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• 2002

In order to darify the neuroprotective effect of Gamibojungikki-tang(GBJIKT) water extract on cultured mouse spinal sensory neuron damaged by glucose Oxidase (GO), NR (Neutral Red) assay and LDH (Lactate Dehydrogenase) activity assay were carried out after the cultured mouse spinal sensory neuron were preincubated with various concentrations of GBJIKT water extract for 3 hours prior to exposure of GO. Cell viability of cultured mouse spinal sensory neurons exposed to various concentrations of GO for 8 hours was decreased in a dose-dependent manner. NR/sub 50/ values were 50 mU/ml GO. Cultured mouse spinal sensory neurons in the medium containing various concentration of GO for 8 hours showed increasing of LDH activity. We knew that GO was toxic on cultured spinal sensory neurons. Pretreatment of GBJIKT water extract for 3 hours following GO prevented the GO-induced neurotoxicity such as increasing of LDH activity. These results suggest that GO shows toxic effect on cultured spinal sensory neurons and GBJIKT water extract is highly effective in proecting the neurotoxicity induced by GO.

• Biomolecules & Therapeutics
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• v.28 no.2
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• pp.152-162
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• 2020

Cerebral ischemia exhibits a multiplicity of pathophysiological mechanisms. During ischemic stroke, the reactive oxygen species (ROS) concentration rises to a peak during reperfusion, possibly underlying neuronal death. Recombinant human erythropoietin (EPO) supplementation is one method of treating neurodegenerative disease by reducing the generation of ROS. We investigated the therapeutic effect of PEGylated EPO (P-EPO) on ischemic stroke. Mice were administered P-EPO (5,000 U/kg) via intravenous injection, and middle cerebral artery occlusion (MCAO) followed by reperfusion was performed to induce in vivo ischemic stroke. P-EPO ameliorated MCAO-induced neurological deficit and reduced behavioral disorder and the infarct area. Moreover, lipid peroxidation, expression of inflammatory proteins (cyclooxygenase-2 and inducible nitric oxide synthase), and cytokine levels in blood were reduced by the P-EPO treatment. In addition, higher activation of nuclear factor kappa B (NF-κB) was found in the brain after MCAO, but NF-κB activation was reduced in the P-EPO-injected group. Treatment with the NF-κB inhibitor PS-1145 (5 mg/kg) abolished the P-EPO-induced reduction of infarct volume, neuronal death, neuroinflammation, and oxidative stress. Moreover, P-EPO was more effective than EPO (5,000 U/kg) and similar to a tissue plasminogen activator (10 mg/kg). An in vitro study revealed that P-EPO (25, 50, and 100 U/mL) treatment protected against rotenone (100 nM)-induced neuronal loss, neuroinflammation, oxidative stress, and NF-κB activity. These results indicate that the administration of P-EPO exerted neuroprotective effects on cerebral ischemia damage through anti-oxidant and anti-inflammatory properties by inhibiting NF-κB activation.

• Korean Journal of Pharmacognosy
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• v.38 no.2 s.149
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• pp.170-175
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• 2007

Activated microglia by neuronal injury or inflammatory stimulation overproduce nitric oxide (NO) by inducible nitric oxide synthase (iNOS) and reactive oxygen species (ROS) such as superoxide anion, resulting in neurodegenerative diseases. The toxic peroxynitrite (ONOO$^-$), the reaction product of NO and superoxide anion further contributes to oxidative neurotoxicity. We tried to evaluate the effects of two kinds of varieties of Perilla frutescens var japnica Hara on the NO production in lipopolysaccharide (LPS)-activated microglia. The perilla cultivars of Namcheondeulkkae (NC) and Boradeulkkae (BR) were developed by pure line from the local variety and by a cross between 'deulkkae' and 'chajogi', respectively. Spirit, hexane, chloroform and butanol fractions of the leaves of NC and BR inhibited the production of NO in LPS-activated microglia. The fractions of BR showed stronger activity than NC and the spirit extracts was the most potent in both cultivars. The solvent fractions of BR suppressed the expression of protein and mRNA of iNOS in LPS-activated microglial cells. Moreover, the extracts of NC and BR showed the activity of peroxynitrite scavenging in cell free bioassay system. These results imply that Namcheondeulkkae and Boradeulkkae might have neuroprotective activity through the inhibition of NO production by activated microglial cells and peroxynitrite scavenging activity.

• Herbal Formula Science
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• v.22 no.1
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• pp.105-112
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• 2014

Background and objective: Methamphetamine (Meth) is a widely abused psychostimulant that produces hyperlocomotion in rodents. Radix of Glycyrrhizae uralensis comprises a variety of bioactive components that have neuroprotective effects. In a previous study, we have demonstrated methanol extracts from radix of Glycyrrhizae uralensis (MEGR) suppress acute cocaine-induced extracellular dopamine release in the nucleus accumbens. In the present study, we investigated the effect of MEGR on acute Meth-induced hyperlocomotion. Methods: Male Sprague-Dawley rats were orally administered with MEGR (60 mg/kg and 180 mg/kg) 60 min prior to an intraperitoneal injection of Meth (1.0 mg/kg). Results: Behavioral analysis showed acute Meth greatly increased locomotor activities, while pretreatment with MEGR dose dependently inhibited the hyperlocomotion. In parallel, there were markedly increased levels of dopamine and its metabolite 3, 4-dihydroxyphenylacetic acid in the nucleus accumbens tissues in Meth-treated rats, which were also almost completely reversed by 180 mg/kg MEGR. Conclusions: These results showed that radix of Glycyrrhizae uralensis attenuates Meth-induced hyperlocomotion by inhibiting dopamine synthesis and utilization, suggesting that radix of Glycyrrhizae uralensis might be effective in blocking the rewarding effect of Meth.

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