• Journal of Microbiology and Biotechnology
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• v.12 no.4
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• pp.691-691
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• 2002

In the course of our screening for neuroprotective agents, a new compound (1) was isolated together with a known compound, caruilignan C (2), from the fruiting body of Daldinia concentrica. Their structures were determined on the basis of various spectral studies. Both compounds exhibited neuroprotective effect against iron-induced neurodegeneration in a primary culture of mouse cortical neurons.

• Journal of Microbiology and Biotechnology
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• v.12 no.4
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• pp.692-694
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• 2002

In the course of our screening for neuroprotective agents, a new compound (1) was isolated together with a known compound, caruilignan C (2), from the fruiting body of Daldinia concentrica. Their structures were determined on the basis of various spectral studies. Both compounds exhibited neuroprotective effect against iron-induced neurodegeneration in a primary culture of mouse cortical neurons.

• Natural Product Sciences
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• v.29 no.1
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• pp.10-16
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• 2023

We previously reported that dried Lysimachia christinae whole plant extract exerted significant neuroprotective activity. In this study, we tried to isolate neuroprotective compounds of L. christinae. We evaluated the neuroprotective activity of the four fractions (hexane, chloroform, ethyl acetate, and n-butanol fractions) of methanol extract. Among them, ethyl acetate and n-butanol fractions showed most potent neuroprotective activity against glutamate excitotoxicity. Nine compounds were isolated from ethyl acetate and n-butanol fractions of L. christinae extract and identified as cynaroside (1), (3,4,5,6-tetrahydroxytetrahydro-2H-pyran-2-yl)methyl-3-hydroxy-2-octyldopentaconta-23,33-dienoate (2), androst-16-ene-3,6-diol (3), 2-hydroxy-24-propoxytetracos-4-enoic acid (4), 2-hydroxy-24-methoxytetracos-4-enoic acid (5), 12-(stearoyloxy)octadec-9-enoic acid (6), β-sitosterol (7), (E)-4-(3,4-dimethoxyphenyl)but-3-en-1-yl palmitate (8) and (1S,2S,3R,4R)-4-(((2S,3R,4R,5R,6S)-2-(((2R,3R,4S,5R,6R)-2-(3,4-dimethoxyphenethoxy)-3,5-dihydroxy-6-(hydroxymethyl) tetrahydro-2H-pyran-4-yl)oxy)-4,5-dihydroxy-6-methyltetrahydro-2H-pyran-3-yl)oxy)cyclohexane-1,2,3-triol (9) by spectroscopic data such as UV, IR, NMR, Mass spectroscopy. Their neuroprotective activity was evaluated by MTT assay. Cynaroside (1) and androst-16-ene-3,6-diol (3) had significant neuroprotective activity against glutamate-injured HT22 cells. The neuroprotective efficacy of cynaroside (1) and androst-16-ene-3,6-diol (3) was related to their anti-oxidative activity.

• Korean Journal of Pharmacognosy
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• v.51 no.1
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• pp.30-35
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• 2020

We previously reported that caffeic acid isolated from Lonicera japonica showed potent neuroprotective activities against glutamate injured neuronal cell death in primary cortical cells. In this study, we tried to confirm the neuroprotective activity in glutamate injured HT22 cells and elucidate mechanisms of neuroprotective action of caffeic acid. We used glutamate induced HT22 cell death as a bioassay system. The compound decreased reactive oxygen species increased by high concentration of glutamate treatment in HT22 cells. Also, Ca²⁺ concentration was decreased by this compound. This compound made mitochondrial membrane potential maintain to normal condition. This also affected anti-oxidative enzymes and glutathione contents. Treatment of this compound increased not only glutathione reductase and peroxidase to the control level and also amount of glutathione, an endogeneous antioxidant. These experimental results showed that caffeic acid isolated from L. japonica exerted potent neuroprotective activity through the anti-oxidative pathway.

• Korean Journal of Pharmacognosy
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• v.50 no.2
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• pp.118-123
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• 2019

Glutamate acts as an important neurotransmitter in brain. However, high concentration of glutamate showed an excitatory neurotoxicity and resulted to neuronal cell death. Neuronal cell death is known for one of the reason of Alzheimer's disease, a neurodegenerative disease. We tried to find neuroprotective medicinal plants by neuroprotection activity against glutamate injured HT22 cells as a model system. In the course of bioscreening of various medicinal plants, Taraxacum platycarpum extract showed significant neuroprotective activity. We tried to elucidate mechanisms of neuroprotective activity. T. platycarpum extract reduced ROS and intracellular $Ca^{2+}$ concentration increased by glutamate induced neurotoxicity. In addition, mitochondrial membrane potential was restored to the control level. Also, glutathione level, glutathione reductase and glutathione peroxidase activity were increased by T. platycarpum extract treatment. These data suggested that T. platycarpum showed neuroprotective activity via antioxidative activity.

• Korean Journal of Pharmacognosy
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• v.53 no.1
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• pp.1-7
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• 2022

In the previous study, we reported that luteolin isolated from Lonicera japonica methanolic extract had potent neuroprotective activities in neuronal cell death injured by excessive glutamate. In this study, we tried to confirm the neuroprotective activities of luteolin in glutamate injured HT22 cells and establish mechanisms of neuroprotective action of luteolin. We used HT22 cell death injured by glutamate as a bioassay system. Luteolin decreased reactive oxygen species increased by excessive glutamate treatment in HT22 cells. Also, Ca²⁺ concentration was decreased by luteolin treatment. Luteolin made mitochondrial membrane potential maintain to normal condition. It also increased not only glutathione reductase but also peroxidase to the control level. And it increased amount of glutathione, an endogenous antioxidant. These results suggested that luteolin isolated from L. japonica showed potent neuroprotective activity through the anti-oxidative pathway.

• Korean Journal of Pharmacognosy
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• v.54 no.1
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• pp.9-15
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• 2023

In the previous study, we reported that cynaroside isolated from Lysimachia christinae methanolic extract had potent neuroprotective activities in neuronal cell death injured by excessive glutamate. In this study, we tried to confirm the neuroprotective activities of cynaroside in glutamate injured HT22 cells and establish mechanisms of neuroprotective action of cynaroside. We employed HT22 cells damaged by glutamate-induced cell death as a bioassay system. Cynaroside decreased reactive oxygen species increased by excessive glutamate treatment in HT22 cells. Also, Ca²⁺ concentration was decreased by cynaroside treatment. Cynaroside restored mitochondrial membrane potential to normal condition. It also increased not only glutathione reductase but also peroxidase to the control level. And it increased amount of glutathione, an endogenous antioxidant. These results suggested that cynaroside isolated from L. christinae showed potent neuroprotective activity through the anti-oxidative pathway.

• Natural Product Sciences
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• v.17 no.1
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• pp.58-63
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• 2011

Insampaedok-san is a traditional medicine used for the treatment of colds. We investigated several compounds in Insampeadok-san, and tested their neuroprotective and anti-oxidative activities after fermentation with Lactobacillus. The amounts of four marker compounds (ferulic acid, hesperidin, 6-gingerol and glycyrrhizin) and unidentified compounds in Insampaedok-san (IS) and fermented Insampaedok-san (FIS) were measured and compared by an established HPLC-DAD method. Neuroprotective activity of IS and FIS extracts was evaluated and compared after glutamate-induced neurotoxicity in HT22 cells. Anti-oxidative activity of IS and FIS was also compared in DPPH free radical, hydroxyl radical and hydrogen peroxide scavenging activity assays. Contents of two compounds, ferulic acid and glycyrrhizin were decreased while 6-gingerol was increased by fermentation. FIS showed more potent neuroprotective activity than IS. DPPH, hydroxyl radical and hydrogen peroxide scavenging was slightly increased by FIS when compared to IS. In conclusion, fermentation with Lactobacillus can vary the amounts of the marker compounds in IS and improve neuroprotective and anti-oxidative activities of IS.

• Korean journal of food and cookery science
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• v.28 no.6
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• pp.821-828
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• 2012

In an attempt to identify the neuroprotective effect of Cudrania tricuspidata (CT) leaves against ROS (reactive oxygen species)-induced oxidative stress in neuronal cells, the extracts from CT leaves were investigated using PC12 cells and N18-RE-105 cells. The methanolic and ethanolic extracts from CT were denoted as CTM (Cudrania tricuspidata Leaves methanolic extracts) and CTE (Cudrania tricuspidata Leaves ethanolic extracts), respectively. The neuroprotective effects of the extracts were measured by DCF-DA assay, MTT reduction assay, and LDH release assay. The PC12 cells exposed to $H_2O_2$-induced oxidative stress and the N18-RE-105 cells exposed to glutamate-induced oxidative stress were treated with various concentrations of CTM and CTE. The results, CTM treatments resulted in the induction of a dose-dependent protective effect in PC12 cells and N18-RE-105 cells. Interestingly, CTE also showed neuroprotective effect in PC12 cells and N18-RE-105 cells. Therefore, these results suggest that CTM and CTE could be a new potential candidate as neuroprotective agents against ROS-induced oxidative stress in neuronal cells.

• Annals of Clinical Neurophysiology
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• v.8 no.1
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• pp.63-70
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• 2006

Background: Testosterone is reported to have neuroprotective effect in various neurological diseases. Recently, the mechanism involved in nitric oxide (NO)-mediated motor neuron death is under extensive investigation. The Cu/Zn-superoxide dismutase (SOD1) mutations has been implicated in selective motor neuron death of amyotrophic lateral sclerosis (ALS) and it is said to play an important role in NO-mediated motor neuron death. However, neuroprotective effect of testosterone on motor neuron exposed to NO has rarely been studied. Methods: Motor neuron-neuroblastoma hybrid cells expressing wild-type or mutant (G93A or A4V) SOD gene were treated with $200{\mu}M$ S-nitrosoglutathione. After 24 hr, cell viability was measured by MTT assay. To see the neuroprotective effect of testosterone, pretreatment with 1 nM testosterone was done 1 hr before S-nitroglutathione treatment. To study the mechanism of protective effect, $20{\mu}M$ flutamide (androgen receptor antagonist) was also pretreated with testosterone 1 hr before S-nitroglutathione treatment. Results: S-nitrosoglutathione showed significant neurotoxic effect in all three cell lines. Percentage of cell death was somewhat different in each cell line. 1 nM testosterone showed neuroprotective effect in G93A and wild-type cell line. In A4V cell line, testosterone did not showed neuroprotective effect. The neuroprotective effect of testosterone was reversed by $20{\mu}M$ flutamide. Conclusions: These results indicate that testosterone induces neuroprotection in NO-mediated motor neuron death directly through the androgen receptor. This neuroprotective effect of testosterone varies according to the types of SOD1 gene mutation. These data suggest that testosterone may be of therapeutic value against ALS.