• Journal of Korean Medicine Rehabilitation
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• v.18 no.4
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• pp.1-11
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• 2008

Objectives : Cerebral ischemia resulting from transient or permanent occlusion of cerebral arteries leads to neuronal cell death and eventually causes neurological impairments. Scrophulariae radix is the roots of Scrophularia buergeria. In the present study, we investigated the effects of the aqueous extract of Scrophulariae radix on apoptotic cell death in the hippocampal dentate gyrus following transient global ischemia in gerbils. Methods : For this study, step-down avoidance task, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and immunohistochemistry for caspase-3 were performed. Results : The present results showed that apoptotic cell death in the hippocampal dentate gyrus was significantly increased following transient global ischemia in gerbils. Treatment with the aqueous extract of Scrophulariae radix suppressed the ischemia-induced apoptosis in the dentate gyrus and thus facilitated the recovery of short-term memory impairment induced by ischemic cerebral injury. Conclusions : Here in this study, we have shown that Scrophulariae radix has a positive effect on-and possesses protective qualities against ischemia-induced apoptotic neuronal cell death, and it can be used for the treatment of ischemic brain diseases.

• Journal of Nutrition and Health
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• v.54 no.6
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• pp.618-630
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• 2021

Purpose: The ginger rhizome (Zingiber officinale) is widely cultivated as a spice for its aromatic and pungent components. One of its constituents, 6-hydroxydopamine (6-OHDA) is usually thought to cross the cell membrane through dopamine uptake transporters, and induce inhibition of mitochondrial respiration and the generation of intracellular reactive oxygen species (ROS). This study examines the neuroprotective effect and acetylcholinesterase (AChE) inhibitory activity of fermented ginger extracts (FGEs) on 6-OHDA induced toxicity in SH-SY5Y human neuroblastoma cells. Methods: Ginger was fermented using 2 species of Bacillus subtilis, with or without enzyme pretreatment. Each sample was extracted with 70% ethanol. Neurotoxicity was assessed by applying the EZ-Cytox cell viability assay and by measuring lactic dehydrogenase (LDH) release. Morphological changes of apoptotic cell nuclei were observed by Hoechst staining. Cell growth and apoptosis of SH-SY5Y cells were determined by Western blotting and enzyme activity analysis of caspase-3, and AChE enzymatic activity was determined by the colorimetric assay. Results: In terms of cell viability and LDH release, exposure to FGE showed neuroprotective activities against 6-OHDA stimulated stress in SH-SY5Y cells. Furthermore, FGE reduced the 6-OHDA-induced apoptosis, as determined by Hoechst staining. The occurrence of apoptosis in 6-OHDA treated cells was confirmed by determining the caspase-3 activity. Exposure to 6-OHDA resulted in increased caspase-3 activity of SH-SY5Y cells, as compared to the unexposed group. However, pre-treatment with FGE inhibited the activity of caspase-3. The neuroprotective effects of FGE were also found to be caspase-dependent, based on reduction of caspase-3 activity. Exposure to FGE also inhibited the activity of AChE induced by 6-OHDA, in a dose-dependent manner. Conclusion: Taken together, our results show that FGE exhibits a neuroprotective effect in 6-OHDA treated SH-SY5Y cells, thereby making it a potential novel agent for the prevention or treatment of neurodegenerative disease.

• Journal of Chest Surgery
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• v.41 no.4
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• pp.405-416
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• 2008

Background: Spinal cord ischemic injury during thoracic and thoracoabdominal aortic surgeries remains a potentially devastating outcome despite using various methods of protection. Neuronal voltage-dependent sodium channel antagonists are known to provide neuroprotection in cerebral ischemic models. This study was designed to compare the neuroprotective effects of phenytoin with those of hypothermia in a rabbit model of spinal cord ischemia. Material and Method: Spinal cord ischemia was induced in New Zealand white rabbits by means of infrarenal aortic cross clamping for 25 minutes. Four groups of 8 animals each were studied. The control group and the hypothermia group received retrograde infusion of saline only ($22^{\circ}C$, 2 mL/min); the normothermic phenytoin group and the hypothermicphenytoin group received retrograde infusion of 100 mg of phenytoin at different rectal temperatures ($39^{\circ}C$ and $37^{\circ}C$, respectively) during the ischemic period. The neurologic function was assessed at 24 and 72 hours after the operation with using the modified Tarlov criteria. The spinal cords were harvested after the final neurologic examination for histopathological examination to objectively quantify the amount of neuronal damage. Result: No major adverse effects were observed with the retrograde phenytoin infusion during the aortic ischemic period. All the control rabbits became severely paraplegic, Both the phenytoin group and the hypothermia group had a better neurological status than did the control group (p < 0.05). The typical morphological changes that are characteristic of neuronal necrosis in the gray matter of the control animals were demonstrated by means of the histopathological examination, whereas phenytoin or hypothermia prevented or attenuated these necrotic phenomena (p < 0.05). The number of motor neuron cells positive for TUNEL staining was significantly reduced, to a similar extent, in the rabbits treated with phenytoin or hypothermia. Phenytoin and hypothermia had some additive neuroprotective effect, but there was no statistical significance between the two on the neurological and histopathological analysis. Conclusion: The neurological and histopathological analysis consistently demonstrated that both phenytoin and hypothermia may afford significant spinal cord protection to a similar extent during spinal cord ischemia in rabbits, although no significant additive effects were noticed.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.7
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• pp.938-947
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• 2016

Antioxidant activities and neuroprotective effects of ethyl acetate fraction from Dendropanax morbifera (EFDM) against high glucose-induced oxidative stress and neurotoxicity were investigated to confirm their physiological activities. An 80% ethanolic extract of D. morbifera showed the highest contents of total phenolic compounds as well as 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) and 1,1-diphenyl-2-picrylhydrazyl radical scavenging activities. The extract was fractionated using several solvents, and the ethyl acetate fraction showed the highest activities in ferric reducing/antioxidant power and malondialdehyde inhibitory assays. To evaluate the neuroprotective effect based on antioxidant activities, cell viability was assessed using PC12 and MC-IXC cells in $H_2O_2$- and high glucose-induced cytotoxic assays, respectively. EFDM evidently showed neuroprotective effects in all cells (neuron-like PC12 cells and human brain-originated neuroblastoma MC-IXC cells). Inhibitory effect of the extract on acetylcholinesterase (AChE) as an acetylcholine-hydrolyzing enzyme was performed to examine the effect on cognitive function. EFDM presented an AChE inhibitory effect. Finally, high-performance liquid chromatography analysis showed that the major phenolic compound of EFDM is probably a rutin.

• Korean Journal of Food Science and Technology
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• v.45 no.3
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• pp.350-355
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• 2013

The quality of fermented dropwort extract (FDE) and fermented dropwort vinegar (FDV) was assessed for free sugar, organic acid and free and total amino acid content. Major organic acids were lactic acid in FDE and acetic acid in FDV. Free sugars in FDE were fructose and glucose, and those in FDV were fructose, sucrose, and maltose. Aspartic acid was the major free amino acid in both FDE and FDV. Additionally, the main free amino acids in FDE were alanine and ${\gamma}$-amino-n-butyric acid (GABA), while those in FDV were arginine and valine. Moreover, to investigate the protective effects of FDE and FDV against oxidative stress induced by t-BHP and $H_2O_2$, C6 cells were treated with FDE or FDV prior to inducing the oxidative damage. FDE and FDV inhibited cell death significantly in a dose-dependent manner. These data imply that FDE and FDV may be effective in neuronal cell protection against oxidative damage.

• Journal of agriculture & life science
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• v.46 no.6
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• pp.137-146
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• 2012

This study investigated whether ferulic acid modulates the heme oxygenase (HO)-1 and HO-2 expression in middle cerebral artery occlusion (MCAO)-induced brain injury. Rats (Sprague-Dawley, male) were treated with vehicle or ferulic acid (100 mg/kg, i.v.) before MCAO, and cerebral cortex tissues were collected 24 h after MCAO. This study clearly confirmed the protective effects of ferulic acid during MCAO-induced damage using hematoxylin and eosin staining. MCAO induces nuclear chromatin condensations and necrotic changes with scalloped shrunken form. However, ferulic acid prevented MCAO-induced histopathological changes. HO-1 and HO-2 expression levels were measured using reverse-transcription PCR and Western blot analyses. HO-1 levels were decreased in vehicle-treated animals after MCAO, whereas this decrease in HO-1 levels was attenuated by ferulic acid treatment. However, the level of HO-2 was consistently maintained in the cerebral cortex of vehicle- and ferulic acid-treated animals after MCAO. These results demonstrated that ferulic acid regulates HO-1 expression in ischemic brain injury, while ferulic acid do not modulate HO-2 expression in MACO. In conclusion, these findings suggest that ferulic acid exerts a neuroprotective effect by preventing the MCAO-induced decrease of HO-1 expression.

• 한국약용작물학회:학술대회논문집
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• 2010.10a
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• pp.406-407
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• 2010

• Journal of Ginseng Research
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• v.24 no.4
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• pp.196-201
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• 2000

Effects of ginsenosides on NaCN-induced neuronal cell death were studied in cultured rat cerebellar granule cells. NaCN produced a concentration-dependent (1-10 mM) reduction of cell viability (measured by frypan blue exclusion test), that was blocked by N-methyl-D-aspartate receptor antagonist (MK-801) and L-type Ca$\^$2+/ channel blocker (verapamil). Pretreatment with ginsenosides (Rb$_1$, Rc, Re, Rf and Rg$_1$) significantly decreased the neuronal cell death in a concentration range of 0.5∼5$\mu\textrm{g}$/ml. Ginsenosides Rb$_1$ and Rc (5 $\mu\textrm{g}$/ml) inhibited glutamate release into medium induced by NaCN (5 mM). NaCN (1 mM)-induced increase of [Ca$\^$2+/], was significantly inhibited by the pretreatment of Rb$_1$ and Rc (5 $\mu\textrm{g}$/ml). Other ginsenosides caused relatively little inhibition on the elevation of glutamate release and of (Ca$\^$2+/). These results suggest that the NaCN-induced neurotoxicity was related to a series of cell responses consisting of glutamate release and [Ca$\^$2+/]i elevation via glutamate (NMDA and kainate) receptors and resultant cell death, and that ginsenosides, especially Rb$_1$ and Rc, prevented the neuronal cell death by the blockade of the NaCN-induced Ca$\^$2+/influx.

• Food Science and Preservation
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• v.20 no.6
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• pp.840-845
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• 2013

This study investigated the effects (i.e., the acetylcholinesterase activity, lipid peroxidation, and neuronal survival) of 20 kinds of medicinal water extracts. The water extracts of three medicinal plants - Cornus officinalis, Glycyrrhiza glabra, and Angelica gigas - were found to be the most effective on acetylcholinesterase inhibitory activity. In the lipid peroxidation-generating system induced by $H_2O_2/FeSO_4$ in rat brain homogenates, Perilla frutescens, Polygonum multiflorum, Cinnamomun cassia, and G. glabra exhibited protective activity against lipid peroxidation. The neuronal cell death induced by L-glutamate in PC12 was suppressed by the water extracts of G. glabra, Cinnamomun cassia, Platycodon grandiflorum, and Mentha arvensis at the concentration of $100{\mu}g/mL$. Taken together, these results showed that the water extract of G. glabra has the potential anti-dementia activity, which suggests that it might provide an effective strategy for improving dementia.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.10 no.3
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• pp.648-653
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• 2009

p62 is a key component of protein aggregates found in brains of neurodegenerative diseases in which oxidative stress is involved in the pathogenesis. p62 was induced in SH-SY5Y, a neuroblastoma cell line, by hydroxydoparnine or $C_2-ceramide$ known to be related to neurodegenerative diseases. The over-expression of p62 showed the neuroprotective effect against the ceramide induced cell death. In addition, p62 became insoluble and cleaved forms as time proceeded after the ceramide treatment, suggesting the mechanism by which p62 is associated with aggregates in neurodegenerative diseases.