• Title/Summary/Keyword: Neuroprotective Effects

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Laccase Fermentation of Clove Extract Increases Content of Dehydrodieugenol, Which Has Neuroprotective Activity against Glutamate Toxicity in HT22 Cells

  • Lee, Han-Saem;Yang, Eun-Ju;Lee, Taeho;Song, Kyung-Sik
    • Journal of Microbiology and Biotechnology
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    • v.28 no.2
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    • pp.246-254
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    • 2018
  • Enzyme fermentation is a type of food processing technique generally used to improve the biological activities of food and herbal medicines. In this study, a Syzygii Flos (clove) extract was fermented using laccase derived from Trametes versicolor (LTV). The fermented clove extract showed greater neuroprotective effects against glutamate toxicity on HT22 than the non-fermented extract did. HPLC analysis revealed that the eugenol (1) and dehydrodieugenol (2) contents had decreased and increased, respectively, after fermentation. The content of 2 peaked at 1 h after fermentation to $103.50{\pm}8.20mg/g_{ex}$ (not detected at zero time), while that of 1 decreased to $79.54{\pm}4.77mg/g_{ex}$ ($185.41{\pm}10.16mg/g_{ex}$ at zero time). Compound 2 demonstrated promising HT22 neuroprotective properties with inhibition of $Ca^{2+}$ influx, the overproduction of intracellular reactive oxygen species, and lipid peroxidation. In addition, LTV showed the best fermentation efficacy compared with laccases derived from Pleurotus ostreatus and Rhus vernicifera.

Neuroprotective Effect of Cirsium japonicum and Silibinin on Lipopolysaccharide-induced Inflammation in BV2 Microglial Cells (대계와 실리비닌의 Mouse BV2 Microglial Cells에서 Lipopolysaccharide에 의해 유발된 염증반응에 대한 신경보호 효과)

  • Yeo, Hyun-Soo;Kim, Dong-Woo;Jun, Chan-Yong;Choi, You-Kyung;Park, Chong-Hyeong
    • The Journal of Internal Korean Medicine
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    • v.28 no.1
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    • pp.166-175
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    • 2007
  • Objectives : This study was designed to evaluate the neuroprotective effect of Cirsium japonicum and Silibinin on lipopolysaccharide-induced inflammation in BV2 microglial cells. Methods : We studied on the neuroprotective effect of lipopolysaccharide-induced inflammation using MTS assay, western blot, and nitric oxide detection on mouse BV2 microglial cells. Results : Cirsium japonicum dose-dependently (50${\mu}g/ml$${\sim}$$250{\mu}g/ml$) inhibited nitrite production and iNOS expression in lipopolysaccharide-induced BV2 microglia and also significantly reduced lipopolysaccharide-induced COX-2 activation in western blot. Silibinin dose-dependently (10${\mu}M$${\sim}$$100{\mu}M$) inhibited nitrite production and iNOS expression in lipopolysaccharide-induced BV2 microglial cells. Silibinin also significantly reduced lipopolysaccharide-induced COX-2 activation in western blot. Conclusion : These effects of neuroprotection related to anti-inflammation suggest that Cirsium japonicum and Silibininmay be useful candidates for the development of a drug for related neurodegenerative diseases.

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The protective effects of ethanolic extract of Clematis terniflora against corticosterone-induced neuronal damage via the AKT and ERK1/2 pathway

  • Noh, Yoohun;Cheon, Seungui;Kim, In Hye;Kim, Inyong;Lee, Seung-Ah;Kim, Do-Hee;Jeong, Yoonhwa
    • BMB Reports
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    • v.51 no.8
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    • pp.400-405
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    • 2018
  • Chronic stress induces neuronal cell death, which can cause nervous system disorders including Parkinson's disease and Alzheimer's disease. In this study, we evaluated the neuroprotective effects of Clematis terniflora extract (CTE) against corticosterone-induced apoptosis in rat pheochromocytoma (PC12) cells, and also investigated the underlying molecular mechanisms. At concentrations of 300 and $500{\mu}g/ml$, CTE significantly decreased apoptotic cell death and mitochondrial damage induced by $200{\mu}M$ corticosterone. CTE decreased the expression levels of endoplasmic reticulum (ER) stress proteins GRP78, GADD153, and mitochondrial damage-related protein BAD, suggesting that it downregulates ER stress evoked by corticosterone. Furthermore, our results suggested that these protective effects were mediated by the upregulation of p-AKT and p-ERK1/2, which are involved in cell survival signaling. Collectively, our results indicate that CTE can lessen neural damage caused by chronic stress.

Neuroprotective effects of vitamin C (비타민 C의 신경 보호 효과)

  • Sim, In-Seop;Lee, Kyeong-Hui;Kim, Eun-Jin;Cha, Myeong-Hun;Kim, Eun-Jeong;Kim, Ga-Min;Kim, Hyeong-A;Lee, Bae-Hwan
    • Proceedings of the Korean Society for Emotion and Sensibility Conference
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    • 2008.10a
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    • pp.147-150
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    • 2008
  • Vitamin C ascorbic acid (AA) and dehydroascorbic acid (DHA) as an antioxidant have been shown to have protective effects in experimental neurological disorder models such as stroke, ischemia, and epileptic seizures. The present study was conducted to examine the protective effect of AA and DHA on Kainic acid (KA) neurotoxicity using organotypic hippocampal slice cultures (OHSC). After 12h KA treatment, significant delayed neuronal death was detected in CA3 region, but not in CA1. Intermediate dose of AA and DHA pretreatment significantly prevented cell death and inhibit ROS level, mitochondrial dysfunction and capase-3 activation in CA3 region. In the case of low or high dose, however, AA or DHA pretreatment were not effective. These data suggest that both AA and DHA pretreatment have neuroprotective effects on KA-induced neuronal injury depending on the concentration, by means of inhibition of ROS generation, mitochondrial dysfunction, and caspase-dependent apoptotic pathway.

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Protein Kinase C-mediated Neuroprotective Action of (-)-epigallocatechin-3-gallate against $A{\beta}_{1-42}$-induced Apoptotic Cell Death in SH-SY5Y Neuroblastoma Cells

  • Jang, Su-Jeong;You, Kyoung-Wan;Kim, Song-Hee;Park, Sung-Jun;Jeong, Han-Seong;Park, Jong-Seong
    • The Korean Journal of Physiology and Pharmacology
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    • v.11 no.5
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    • pp.163-169
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    • 2007
  • The neurotoxicity of amyloid $\beta(A\beta)$ is associated with an increased production of reactive oxygen species and apoptosis, and it has been implicated in the development of Alzheimer's disease. While(-)-epigallocatechin-3-gallate(EGCG) suppresses $A\beta$-induced apoptosis, the mechanisms underlying this process have yet to be completely clarified. This study was designed to investigate whether EGCG plays a neuroprotective role by activating cell survival system such as protein kinase C(PKC), extracellular-signal-related kinase(ERK), c-Jun N-terminal kinase(JNK), and anti-apoptotic and pro-apoptotic genes in SH-SY5Y human neuroblastoma cells. One ${\mu}M\;A{\beta}_{1-42}$ decreased cell viability, which was correlated with increased DNA fragmentation evidenced by DAPI staining. Pre-treatment of SH-SY5Y neuroblastoma cells with EGCG($1{\mu}M$) significantly attenuated $A{\beta}_{1-42}$-induced cytotoxicity. Potential cell signaling candidates involved in this neuroprotective effects were further examined. EGCG restored the reduced PKC, ERK, and JNK activities caused by $A{\beta}_{1-42}$ toxicity. In addition, gene expression analysis revealed that EGCG prevented both the $A{\beta}_{1-42}$-induced expression of a pro-apoptotic gene mRNA, Bad and Bax, and the decrease of an anti-apoptotic gene mRNA, Bcl-2 and Bcl-xl. These results suggest that the neuroprotective mechanism of EGCG against $A{\beta}_{1-42}$-induced apoptotic cell death includes stimulation of PKC, ERK, and JNK, and modulation of cell survival and death genes.

Neuroprotective and Free Radical Scavenging Activities of Phenolic Compounds from Hovenia dulcis

  • Li, Gao;Min, Byung-Sun;Zheng, Chang-Ji;Lee, Joong-Ku;Oh, Sei-Ryang;Ahn, Kyung-Seop;Lee, Hyeong-Kyu
    • Archives of Pharmacal Research
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    • v.28 no.7
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    • pp.804-809
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    • 2005
  • The EtOAc-soluble fraction from a methanolic extract of Hovenia dulcis Thunb. exhibited neuroprotective activity against glutamate-induced neurotoxicity in mouse hippocampal HT22 cells. The neuroprotective activity-guided isolation resulted in 8 phenolic compounds (1-8), such as vanillic acid (1), ferulic acid (2), 3,5-dihydroxystilbene (3), (+)-aromadendrin (4), methyl vanillate (5), (-)-catechin (6), 2,3,4-trihydrobenzoic acid (7), and (+)-afzelechin (8). Among these, compounds 6 and 8 had a neuroprotective effect on the glutamate-induced neurotoxicity in HT22 cells. Furthermore, compound 6 had a DPPH free radical scavenging effect with an $IC_{50}$ value of $57.7{\mu}M$, and a superoxide anion radical scavenging effect with an $IC_{50}$ value of $8.0{\mu}M$. Both compounds 6 and 8 had ABTS cation radical scavenging effects with $IC_{50}$ values of $7.8{\mu}M\;and\;23.7${\mu}M$, respectively. These results suggest that compounds 6 and 8 could be neuroprotectants owing to their free radical scavenging activities.

Neuroprotective Effect of β-Lapachone in MPTP-Induced Parkinson's Disease Mouse Model: Involvement of Astroglial p-AMPK/Nrf2/HO-1 Signaling Pathways

  • Park, Jin-Sun;Leem, Yea-Hyun;Park, Jung-Eun;Kim, Do-Yeon;Kim, Hee-Sun
    • Biomolecules & Therapeutics
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    • v.27 no.2
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    • pp.178-184
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    • 2019
  • Parkinson's disease is a neurodegenerative disease characterized by the progressive loss of dopaminergic neurons within the substantia nigra pars compacta. In the present study, we investigated whether ${\beta}-Lapachone$ (${\beta}-LAP$), a natural naphthoquinone compound isolated from the lapacho tree (Tabebuia avellanedae), elicits neuroprotective effects in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease mouse model. ${\beta}-LAP$ reduced the tyrosine hydroxylase (TH)-immunoreactive fiber loss induced by MPTP in the dorsolateral striatum, and alleviated motor dysfunction as determined by the rotarod test. In addition, ${\beta}-LAP$ protected against MPTP-induced loss of TH positive neurons, and upregulated B-cell lymphoma 2 protein (Bcl-2) expression in the substantia nigra. Based on previous reports on the neuroprotective role of nuclear factor-E2-related factor-2 (Nrf2) in neurodegenerative diseases, we investigated whether ${\beta}-LAP$ induces upregulation of the Nrf2-hemeoxygenae-1 (HO-1) signaling pathway molecules in MPTP-injected mouse brains. Western blot and immunohistochemical analyses indicated that ${\beta}-LAP$ increased HO-1 expression in glial fibrillary acidic protein-positive astrocytes. Moreover, ${\beta}-LAP$ increased the nuclear translocation and DNA binding activity of Nrf2, and the phosphorylation of upstream adenosine monophosphate-activated protein kinase (AMPK). ${\beta}-LAP$ also increased the localization of p-AMPK and Nrf2 in astrocytes. Collectively, our data suggest that ${\beta}-LAP$ exerts neuroprotective effect in MPTP-injected mice by upregulating the p-AMPK/Nrf2/HO-1 signaling pathways in astrocytes.

The Antioxidative and Neuroprotective Effect of Guibi-tang(Guipitang) and Guibi-tang gamibang(Guipitang jiaweijang) on PC12 cells. (귀비탕(歸脾湯)과 귀비탕가미방(歸脾湯加味方)의 항산화 효과 및 6-Hydroxydopamine에 대한 PC12 세포 보호효과 비교연구)

  • Lim, Jae-Whan;Kim, Jong-Woo;Chung, Sun-Yong;Cho, Sung-Hoon;Oh, Myung-Sook;Hwang, Wei-Wan
    • Journal of Oriental Neuropsychiatry
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    • v.20 no.1
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    • pp.1-19
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    • 2009
  • Objectives : This Study was performed to assess the antioxidative and neuroprotective effect of Guibi-tang(Guipi-tang) and Guibi-tang gamibang(Guipitang jiaweifang) on PC12 cells. Methods : The antioxidative effect was investigated through the DPPH radical and ABTS cation scavenging methods and total polyphenol amount of Guibi-tang(Guipitang) and Guibi-tang gamibang(Guipitang jiaweifang). The neuroprotective effect of Guibi-tang(Guipitang) and Guibi-tang gamibang(Guipitang jiaweifang) was assessed using MTT assay in PC12 cells. The scavenging effect of Guibi-tang(Guipitang) and Guibi-tang gamibang(Guipitang jiaweifang) on NO and ROS production induced by 6-OHDA in PC12 cells was evaluated, as well as the attenuating effect of Guibi-tang gamibang(Guipitang jiaweifang) on GSH reduction. Results : 1. Guibi-tang(Guipitang) and Guibi-tang gamibang(Guipitang jiaweifang) had concentration-dependent scavenging activities of DPPH radical 2. Guibi-tang(Guipitang) and Guibi-tang gamibang(Guipitang jiaweifang) had concentration-dependent scavenging activities of ABTS cation. 3. Total polyphenol amount of Guibi-tang(Guipitang) and Guibi-tang gamibang(Guipitang jiaweifang) was calculated 79.10${\pm}$2.20 pg/IO mg and 121.03${\pm}$1.11 pg/IO mg, respectively. 4. Cell viability of Guibi-tang(Guipitang) was increased in a dose dependent manner. Guibi-tang gamibang(Guipitang jiaweifang) was increased at low concentrations, but decreased at high concentrations. 5. In Guibi-tang(Guipitang), cell viability of PC12 cell treated with 6-OHDA was decreased by pre-treatment, and increased by post- and co- treatment. Cell viability of Guibi-tang gamibang(Guipitang jiaweifang) showed variable effects by pre-treatment, but increased by post- and co- treatment. 6. NO production rate of Guibi-tang(Guipitang) didn't show a significant effect, but that of Guibi-tang gamibang(Guipitang jiaweifang) was decreased in a dose dependent manner. 7. ROS production rate of Guibi-tang(Guipitang) was decreased at some concentrations. In Guibi-tang gamibang(Guipitang jiaweifang), ROS production rate was decreased at high concentrations. 8. Guibi-tang gamibang(Guipitang jiaweifang) protected the 6-OHDA-induced GSH reduction. Conclusions : These results demonstrate that both Guibi-tang(Guipitang) and GBTGMB have antioxidative and neuroprotective effect, but Guibi-tang gamibang(Guipitang jiaweifang) has more antioxidative and neuroprotective effect than Guibi-tang.

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Antioxidant activity and neuroprotective effects of ethanol extracts from the core of Diospyros kaki (감 심지 에탄올 추출물의 항산화 활성 및 신경세포 보호 효과)

  • Byun, Eui-Baek;Kim, Min-Jin;Kim, Soon-Jung;Oh, Nam-Soon;Park, Sang-Hyun;Kim, Woo Sik;Song, Ha-Yeon;Han, JeongMoo;Kim, Kwangwook;Byun, Eui-Hong
    • Korean Journal of Food Science and Technology
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    • v.52 no.1
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    • pp.60-66
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    • 2020
  • This study examined the antioxidant activity and neuroprotective effects of ethanol extracts obtained from Diospyros kaki core (DCE). The total polyphenol and flavonoid contents in DCE was 786.47±15.27 and 31.14±0.82 mg/g, respectively. In addition, DCE exhibited a dose-dependent induction of radical scavenging activity, determined by 1,1-diphenyl-picrylhydrazyl (DPPH), 2,2'-azino-bis-(3-ethylbenzothiazoline-6-sulfonicacid) (ABTS), ferric reducing antioxidant power (FRAP), and reducing power assays. The viability of HT22 hippocampal cells was examined to investigate the neuroprotective effect of DCE. DCE treatment did not induce cytotoxicity at concentrations below 1,000 ㎍/mL. Additionally, DCE treatment in the background of H2O2 induce oxidative stress revealed a significant increase in the survival rat, indicated by increased SOD activity and decreased levels of MDA, a lipid peroxidation product. Therefore, the results suggest that DCE can be used as a source of natural antioxidants source and a therapeutic agent for the treatment of brain disorders induced by oxidative stress and neuronal damage.

Neuroprotective Effects of Neutral Pharmacopuncture for Blood Stasis and Tangguisusangami-tang(dangguixusanjiawei-tang ) in the Experimental Traumatic Brain Injury Rats (중성어혈(中性瘀血) 약침(藥鍼)과 당귀수산가미탕(當歸鬚散加味湯)이 외상성 뇌손상 흰쥐의 신경보호에 미치는 영향)

  • Jong, Il-Moon;Choi, Jin-Bong
    • Journal of Korean Medicine Rehabilitation
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    • v.20 no.1
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    • pp.13-26
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    • 2010
  • Objectives : This study was designed to evaluate neuroprotective effects of Neutral Pharmacopuncture for Blood Stasis(NPBS) into SP10 and Tangguisusangami-tang (dangguixusanjiawei-tang)(TGT) in the experimental Traumatic Brain Injury(TBI)rats. Methods : Male rats were divided into 4 groups. Group I was no treatment after TBI. Group II was treatment with NPBS into SP10 after TBI. Group III was treatment with TGT after TBI. Group IV was NPBS into SP10 and TGT after TBI. The author carried out neurological motor behavioral, histological assessment test. Results : 1. In neurological motor behavior tests, motor and cognitive function recovery was significantly increased in the Group II, III, IV. Also Group IV was increased as compared with Group II, III. 2. In BAX expression, according to priority Group IV, III, II, I were decresed in 7 and 14 days later. Especially Group IV was significantly decreased in 14 days later. 3. In BCL-2 expression, Group IV was increased slightly in 7 days later. Most incresed expression was experimented in the Group IV in 14 days later. 4. In TUNEL expression, IV was decreased as compared with each Group I, II, III in 7 days later. Group IV, III were decreased as compared with each Group I, II, III in 14 days later. Conclusions : According to the results, NPBS and TGT can inhibit apoptosis of cells after TBI in rats by contol of BAX and BCL-2, TUNEL expression. And also can help neurological motor behavioral function.