• 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.

• 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.14 no.2
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• pp.213-219
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• 2007

To develop an anti-dementia agent with potential therapeutic value in the protection of neuronal cells, we selected a water extract of Helianthus annuus seed for analysis. We measured acetylcholinesterase inhibitory activity in the extract, and analyzed the protective effect of the extract on neuronal cell death induced by hydrogen peroxide, or amyloid ${\beta}-peptide$, of SH-SY5Y neuroblastoma cells. The result showed that the extinct exerted protective effects of 83%, 72% and 53% respectively, on cell death induced by 100M, 200M, and 500M hydrogen peroxide. Also, when 50M of amyloid ${\beta}-peptide$ was added to the cells, the extract showed a protective effect (up to 80%) on cell death. Overall, the results showed that the H. annuus extract inhibited acetylcholinesterase activity in a dose-dependent manner, and the extract also strongly protected against cell death induced by hydrogen peroxide or amyloid ${\beta}-peptide$.

• Proceedings of the Korean Journal of Food and Nutrition Conference
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• 2003.07a
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• pp.82-82
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• 2003

오디는 옛부터 보혈자음(補血滋陰), 생진윤조(生津閏操), 현훈이명(眩最耳鳴), 심계실면(心悸失眠), 수발조백(鬚髮早白) 등을 치료하는 효능을 가진다고 알려져 있다. 상심자(桑 子)라 하여 뽕나무 열매로서 한방에서 상심(桑 ), 상실(桑實), 오심(烏 ), 흑심(黑 ) 등으로 지칭되며, 뽕나무과(Moraceae)에 속하는 뽕나무(Morus alba L)의 성숙한 과실로 취화과(聚花果)에 속하며 작은 수과(瘦果)가 많이 모여 이루어진 장원형으로 길이 1 내지 2 cm, 지름 0.5 내지 0.8 cm이며 황갈색, 갈홍색 또는 암자색을 띠고 짧은 줄기가 있다. 작은 수과(瘦果)는 난원형으로 조금 납작한 편이며, 길이는 약 2 mm, 너비는 약 1 mm 이고 육질의 화편(花片) 4개가 둘러싸고 있다. 그러나 아직까지는 오디에 대하여 자연과학적인 연구방법을 이용하여 구체적으로 연구된 바가 많지 않다. 또한 이의 생리활성 성분에 대해서도 그 작용과 연관지어 보고된 바가 많지 않다. 뇌졸중 가운데 뇌조직으로 가는 혈액 공급의 감소 혹은 차단으로 발생되는 허혈성 뇌졸중(ischemic stroke)은 전체 뇌졸중 환자의 약 80%정도를 차지하고 있으나 아직까지 뇌신경세포 손상기전의 복잡성 등으로 뇌졸중으로 발생하는 뇌신경세포의 손상을 보호해 줄 수 있는 물질이 개발되어 있지 못한 실정이다. 한편, 천연물로부터 뇌허혈 보호작용을 가지는 물질의 도출은 주로 한방에서 처방을 중심으로 이루어지고 있으며, 따라서 처방으로부터 신경보호작용을 가지는 물질의 도출은 그 처방에 함유되어 있는 각종 생약이 갖는 다양한 활성으로 인해 어려운 점이 있으며, 비록 효과가 있다고 하더라도 과학적인 입증자료가 매우 미비한 실정이다. 이에 본 연구에서는 위에 언급된 자료를 토대로 오디추출물이 뇌허혈에 효과가 있을 것이라는 가정하에 in vitro system을 이용하여 오디추출물의 신경보호작용기전을 검색하고자 DPPH radical 의 생성억제효과, PC12 cell line을 이용한 산화적 스트레스에 의한 오디추출물의 방어효과, LSP에 의하여 활성화된 BV-2 cell에 미치는 영향 등을 검색하였다. 오디의 DPPH 소거활성은 단일화랍물인 bacicalein과 유사한 효과를 나타냈으며 PC12 cell line을 이용한 산화적 스트레스에 의한 오디의 방어 효과는 LDH activity를 행한 결과 농도 의존적으로 LDH 유리 량을 감소시켰다. 뇌손상시에 오디추출물의 염증방어 효과를 관찰하기 위하여 microglial cell line인 BV2 세포주를 선택하여 배양한 후 LPS로 자극을 준 후 일차적인 염증지표인 NO양을 측정한 결과 BV2 cell에 LPS 100 ng/ml을 처리하는 경우 nitrite량이 유의적으로 증가하였는데 이때 오디추출물을 1, 5, 10 ug/ml의 용량으로 처리하는 경우 역시 저농도에서 NO생성량을 감소시켰다. 정리해보면 뽕나무과 식물인 오디는 신경보호효과가 있는 것으로 사료되는데 이러한 효과는 아마도 오디의 항산화효과에 기인한 것으로 추정된다.

• Korean Journal of Food Science and Technology
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• v.47 no.5
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• pp.673-679
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• 2015

In vitro antioxidant activities and neuronal cell protective effects of the ethyl acetate fraction of a new green extract (Brassica oleracea var. botytis aut italiana) against $H_2O_2$-induced oxidative stress were investigated, and its industrial feasibility was evaluated. The extract showed the highest contents of total phenolic compounds among other extracts as well as a 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) diammonium salt (ABTS) radical scavenging activity and malondialdehyde (MDA) inhibitory effect. This extract not only decreased the intracellular reactive oxygen (ROS) level but also protected the neuronal cells against $H_2O_2$-induced oxidative stress. On analysis using gas chromatograph-mass spectrometry, the following phenolic compounds were identified: quinic acid, ferulic acid, and caffeic acid. Collectively, these results suggest that this new green extract could contain functional substances that would help prevent the risk of neurodegenerative disease.

• Korean Journal of Food Science and Technology
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• v.49 no.5
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• pp.524-531
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• 2017

The study aimed to investigate the antioxidant activity and neuroprotective effect of the ethyl acetate fraction from Orostachys japonicus A. Berger extract (EFOJ) and its main constituent compounds. Among all fractions, the highest content of total phenolics was found in EFOJ. The antioxidant activity of EFOJ was confirmed through the 2,2-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS), 1-1-diphenyl-2-picryl-hydrazyl (DPPH), ferric reducing antioxidant power (FRAP) assays and the inhibitory effect of malondialdehyde (MDA). In addition, we ascertained that EFOJ not only decreased the intracellular ROS level, but also protected the neuronal cells against $H_2O_2$-induced oxidative stress. In liquid chromatography-mass spectrometry analysis, the following were found to be the main compounds of EFOJ: quercetin-3-O-glucoside, kaempferol-3-O-rutinoside, kaempferol-3-O-glucoside, and kaempferol-3-O-rhamnoside. Consequently, these results suggested that the protective effect on neuronal cells was based on the antioxidant activities of the physiologically active compounds of Orostachys japonicus A. Berger extract, which could therefore help to mitigate neurodegenerative diseases.

• Korean Journal of Food Science and Technology
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• v.53 no.4
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• pp.423-433
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• 2021

This study was performed to examine the neuroprotective effect of the ethyl acetate fraction from Eucommia ulmoides oliver leaf (EFEL) on PM_2.5-induced cytotoxicity. EFEL had higher total phenolic and flavonoid contents than the other fractions. In ABTS and DPPH radical scavenging activities, the IC₅₀ of EFEL was measured as 212.80 and 359.13 ㎍/mL, respectively. To investigate the neuroprotective effect of EFEL, MTT and DCF-DA assays were performed on HT22, MC-IXC, and BV-2 cells. EFEL effectively decreased PM_2.5-induced intercellular reactive oxygen species (ROS) content and inhibited PM_2.5-induced cell death. In the results of protein expression related to cellular cytotoxicity on microglial cells (BV-2), EFEL had an improvement effect on cell apoptosis and inflammatory pathways. Rutin and chlorogenic acid were identified as the main physiological compounds. Moreover, it was expected that EFEL, including rutin and chlorogenic acid, could be functional food substances with neuroprotective effects against PM_2.5-induced oxidative stress.

• 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.

• Korean Journal of Food Science and Technology
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• v.49 no.2
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• pp.222-227
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• 2017

Red ginseng prepared from fresh 6-year-old ginseng treated with colloidal gold nanoparticles was extracted using hot water to evaluate its total phenolic and flavonoid contents, antioxidant capacity, and neuroprotective effects. Water extract of red ginseng treated with gold nanoparticles (WERGGN) had total phenolic and total flavonoid contents of 212.2 mg gallic acid equivalents/$^{\circ}Bx$ and 3.5 mg catechin equivalents/$^{\circ}Bx$, respectively. The antioxidant capacities of WERGGN measured using ABTS, DPPH, and ORAC assays were 272.3, 141.2, and 868.4 mg vitamin C equivalents/$^{\circ}Bx$, respectively. The WERGGN showed protective effects on the viability of neuron-like PC-12 cells against oxidative stress induced by hydrogen peroxide in a dose-dependent manner, partly because of a reduction in intracellular oxidative stress. Acetylcholinesterase and butyrylcholinesterase, which degrade the neurotransmitter acetylcholine to terminate neurotransmission, were inhibited by treatment with WERGGN. These results suggest that WERGGN is useful as a functional material to decrease oxidative stress and neuronal damage.

• Journal of agriculture & life science
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• v.44 no.4
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• pp.45-55
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• 2010

In this study, the acetylcholinesterase (AChE) inhibition and neuronal cell protective effects of water, 100% methanol and dichlromethane extracts from garlic were investigated. We found that dichloromethane extract of garlic resulted in a dose-dependent manner on AChE inhibition ($IC_{50}$: $36.1{\mu}g/mL$). In cell viability assay using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide (MTT), cell viabilities of water, 100% methanol and dichlromethane extracts were lower (almost under 40%) than amyloid ${\beta}$ protein ($A{\beta}$)-induced neurotoxicity. Because $A{\beta}$ is also known to increase neuronal cell membrane breakdown, neuronal apoptosis was further confirmed by lactate dehydrogenase (LDH) and neutral red uptake (NRU) assay. Water extract presented relative protection against $A{\beta}$-induced membrane damage in LDH assay. However all garlic extracts showed significant problem with decrease of cell viability in NRU assay, especially at dichloromethan extract. To determine active compounds in column fractions (98:2 fraction) from dichloromethane extract which showed significant AChE inhibitory effect, we performed HPLC and LC-MS analysis. It was supposed that garlic may contain allyl methyl disulfide, diallyl monosulfide, and diallyl disulfide as active compounds.