• 동의생리병리학회지
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• 제21권4호
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• pp.921-933
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• 2007

This experiment was designed to investigate the effects of the KBCMT hot water extract & ultra-fine powder on Alzheimer's Disease Model Induced by ${\beta}A$. The effects of the KBCMT hot water extract on expression of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, NOS-II, COX-2 mRNA and production of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, NO in BV2 microglial cell line treated by lipopolysacchaide(LPS). The effects of the KBCMT hot water extract & ultra-fine powder on (1) the behavior (2) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, CD68 and CD11b; (3) AChE in serum (4) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. The KBCMT hot water extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ mRNA in BV2 microglia cell line treated with LPS. The KBCMT hot water extract suppressed the production of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, NO in BV2 microglial cell line treated with LPS. The KBCMT hot water extract & ultra-fine powder a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured stop-through latency and distance movemet-through latency The KBCMT ultra-fine powder suppressed the expression of TNF-a protein significantly in the microglial cell of mice with Alzheimer's disease induced by ${\beta}A$. The KBCMT hot water extract & ultra-fine powder reduced the MDA and suppressed the over-expression of CD68, CD11b in the mice with Alzheimer's disease induced by ${\beta}A$. The KBCMT hot water extract & ultra-fine powder decreased AChE significantly in the serum of the mice with Alzheimer's disease induced by ${\beta}A$. The KBCMT hot water extract & ultra-fine powder reduced infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. The KBCMT hot water extract & ultra-fine powder reduced the tau protein, GFAP, and presenilin1, 2 of hippocampus in the mice with Alzheimer's disease induced by ${\beta}A$. These results suggest that the KBCMT hot water extract & ultra-fine powder may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the KBCMT hot water extract & ultra-fine powder for Alzheimer's disease is suggested for future research.

• 동의생리병리학회지
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• 제21권3호
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• pp.688-699
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• 2007

This experiment was designed to investigate the effect of the SST hot water extract & ultra-fine Powder on Alzheimer's Disease Model Induced by ${\beta}$A. The effects of the SST hot water extract on expression of IL-1${\beta}$, IL-6, TNF-${\alpha}$, NOS-II, COX-2 mRNA and production of IL-l${\beta}$, IL-6, TNF-${\alpha}$, NO in BV2 microglial cell line treated by lipopolysacchaide(LPS). The effects of the SST hot water extract & ultra-fine powder on (1) the behavior (2) expression of IL-1${\beta}$, TNF-${\alpha}$, MDA, (3) Glucose, AChE in serum (4) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}$A were investigated. The SST hot water extract suppressed the expression of IL-1${\beta}$, IL-6 and TNF-a mRNA ${\alpha}$in BV2 microglia cell line treated with LPS. The SST hot water extract suppressed the production of IL-1${\beta}$, IL-6, TNF-${\alpha}$, NO in BV2 microglial cell line treated with LPS. The SST hot water extract & ultra-fine powder a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}$A in the Morris water maze experiment, which measured stop-through latency. The SST ultra-fine powder suppressed the expression of TNF-a protein significantly in the microglial cell of mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder reduced the MDA and suppressed the over-expression of CD68, CD11b in the mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder decreased AChE significantly in the serum of the mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder reduced infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder reduced the tau protein, GFAP, and presenilin1, 2 of hippocampus in the mice with Alzheimer's disease induced by ${\beta}$A. These results suggest that the SST hot water extract & ultra-fine powder may be effective for the prevention and treatment of A1zheimer's disease. Investigation into the clinical use of the SST hot water extract & ultra-fine powder for Alzheimer's disease is suggested for future research.

• 동의생리병리학회지
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• 제22권5호
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• pp.1315-1321
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• 2008

본 논문은 오랫동안 민간요법으로 염증치료에 사용되어오던 섬수가 lipopolysaccharide(LPS)-자극된 BV2 소교 세포의 nitric oxide(NO) 분비에 미치는 효과에 대해 연구한 내용이다. 실험 결과 섬수는 세포 생존력에 대한 영향 없이 BV2 소교 세포에서 NO 분비를 억제시켰고, nitric oxide synthase (iNOS) 단백질도 감소시켰다. 또한 섬수는 prostaglandin E2 (PGE2) 생산 및 cyclooxygenase (COX)-2 발현을 저지하였고, proinflammatory cytokines과 ${IkB-\alpha}$감소를 억제시켰다. 따라서 섬수가 $I{\kappa}B-{\alpha}$감소를 억제함으로써 NO 합성을 저해하여 항염증작용을 할 수 있다는 내용이다.

• 대한본초학회지
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• 제24권4호
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• pp.173-179
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• 2009

Objectives : In this study, the effects of different fractions isolated from modified Boyanghwanotang(mBHT) extract on LPS-induced inflammation in BV2 microglial cells were investigated. Methods : mBHT was extracted with water, and then fractionated with n-hexane, methylene chloride, ethylacetate and n-butanol. BV2 cells, a mouse microglia line were incubated with different concentrations of each fraction of mBHT for 30 min, and then stimulated with LPS for 24 h. Cell toxicity was determined by MTT assay. The concentration of nitric oxide (NO) was measured in culture medium by Griess reagent assay. The expression of inducible nitric oxide synthease (iNOS) protein was determined by Western blot. Results : Four fractions of mBHT were significantly inhibited LPS-induced NO productions in BV2 cells in a dose-dependent manner. The methylene chloride fraction of mBHT was most strongly inhibited the NO production compared with those of the others. The methylene chloride fraction of mBHT was also suppressed LPS-induced iNOS expression comparison of other fractions at same concentration ($50\;{\mu}g/ml$) in BV2 cells. Conclusions : The results showed that the methylene chloride fraction of mBHT may have an strong anti-inflammatory property through the inhibition of NO production and iNOS expression in activated microglia, and could a therapeutic potential for the treatment of various brain inflammatory diseases.

• 동의신경정신과학회지
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• 제19권2호
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• pp.77-93
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• 2008

Objective : This experiment was designed to investigate the effect of the CBD hot water extract & ultra-fine Powder on Alzheimer's Disease Model Induced by ${\beta}A$. Method : The effects of the CBD hot water extract on expression of interleukin-1 beta($IL-1{\beta}$), $TNF-{\alpha}$ mRNA and production of IL-6, $TNF-{\alpha}$ in BV2 microglial cell line treated by lipopolysacchaide(LPS). The effects of the CBD hot water extract & ultra-fine powder on (1) the behavior (2) expression of $IL-1{\beta}$, tumor necrosis factor-alpha($TNF-{\alpha}$), (3) the infarction area of the hippocampus in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. Result : The CBD hot water extract suppressed the expression of $IL-1{\beta}$, $TNF-{\alpha}$ mRNA in BV2 microglia cell line treated with LPS. The CBD hot water extract significantly suppressed the production of $IL-1{\beta}$, $TNF-{\alpha}$ in BV2 microglial cell line treated with LPS. The CBD hot water extract & ultra-fine powder a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured step-through latency and distance movement-through latency. The CBD hot water extract & ultra-fine powder significantly suppressed the expression of $IL-l{\beta}$ and $TNF-{\alpha}$ protein in the microglial cell of mice with Alzheimer's disease induced by ${\beta}A$. The CBD hot water extract & ultra-fine powder suppressed the over-expression of AChE activity in the serum of the mice with Alzheimer's disease induced by ${\beta}A$. The CBD hot water extract & ultra-fine powder reduced infarction area of hippocampus, in the mice with Alzheimer's disease induced by ${\beta}A$. Conclusions : These results suggest that the CBD hot water extract & ultra-fine powder may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the CBD hot water extract & ultra-fine powder for Alzheimer's disease is suggested for future research.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2018년도 춘계학술발표회
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• pp.92-92
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• 2018

Solanum nigrum L. (SNL), generally known as black nightshade, is traditionally used as medicine to reduce inflammation caused by several diseases like asthma, chronic bronchitis and liver cirrhosis. In this study, anti-inflammatory effects of SNL extract were examined and possible molecular mechanisms of the anti-inflammatory effects were investigated. The inhibitory effects of SNL extract on nitric oxide (NO), pro-inflammatory cytokines ($TNF-{\alpha}$, IL-6) and Matrix metallopeptidase 9 (MMP-9) productions were dissected using lipopolysaccharide (LPS) stimulated murine macrophage-like cell line Raw264.7 cells and human microglial cell line BV2 cells. We further investigated whether SNL extract could suppress the phosphorylation of ERK1/2, JNK, and p38 and the nuclear expression of nuclear factor $NF-{\kappa}B$ p65 in LPS-stimulated Raw264.7 cells and BV2 cells. As a result, we showed that the SNL extract significantly decreased the production of pro-inflammatory cytokines, NO, and MMP-9. In addition, the SNL strongly inhibited the phosphorylation of ERK1/2, JNK, p38 and nuclear translocation of $NF-{\kappa}B$ p65 in activated cells. We confirmed that the extracts of SNL effectively inhibits the anti-inflammatory and may be used as a therapeutic to various inflammatory diseases.

• 동의신경정신과학회지
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• 제21권2호
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• pp.171-189
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• 2010

Objectives : This research investigates the effect of the HBSBS on Alzheimer's disease. Specifically, the effects of the HBSBS extract on (1) the behavior (2) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's disease mice induced with $\beta$A were investigated. Methods : The effects of the HBSBS extract suppressed the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ and NOS-II mRNA in BV2 microglial cell line treated with LPS plus $\beta$A were investigated. The effects of the HBSBS extract on the behavior of the memory deficit mice induced by scopolamine were investigated. Results : 1. The HBSBS extract suppressed the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ and NOS-II mRNA in BV2 microglial cell line treated with LPS plus $\beta$A. 2. The HBSBS extract suppressed the expression of $\beta$A protein production in BV2 microglial cell line treated with LPS plus $\beta$A. 3. The HBSBS extract showed significantly inhibitory effect on the scopolamine-induced impairment of memory in the experiment of Morris water maze. 4. The HBSBS group suppressed the over-expression of IL-1$\beta$ protein, TNF-$\alpha$ protein significantly in the mice with Alzheimer's disease induced by $\beta$A. 5. The HBSBS group reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by $\beta$A. 6. The HBSBS group reduced tau protein, and GFAP in the brain tissue of the mice with AD induced by $\beta$A. Conclusions : These results suggest that the HBSBS group may be effective for the treatment of AD. Thus, HBSBS could be considered among the future therapeutic drugs indicated for the treatment of AD.

• Animal cells and systems
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• 제9권2호
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• pp.101-105
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• 2005

[ ${\beta}ig-h3$ ] is a secretory protein that is induced by $TGF-{\beta}$ and implicated in various disease conditions including fibrosis. We have previously reported that ${\beta}ig-h3$ expression is implicated in astrocyte response to brain injury. In this study, we further investigated potential roles of ${\beta}ig-h3$ protein in the injured central nervous system (CNS). We specifically assessed whether the treatment of microglial cells with ${\beta}ig-h3$ can regulate microglial activity. Microglial cells are the prime effector cells in CNS immune and inflammatory responses. When activated, they produce a number of inflammatory mediators, which can promote neuronal injury. We prepared conditioned medium from the stable CHO cell line transfected with human ${\beta}ig-h3$ cDNA. We then examined the effects of the conditioned medium on the LPS- or $IFN-{\gamma}-mediated$ induction of proinflammatory molecules in microglial cells. Preincubation with the conditioned medium significantly attenuated LPS-mediated upregulation of $TNF-{\alpha},\;IL-1{\beta}$, iNOS and COX-2 mRNA expression in BV2 murine microglial cells. It also reduced $IFN-{\gamma}-mediated$ upregulation of $TNF-{\alpha}$ and COX-2 mRNA expression but not iNOS mRNA expression. Assays of nitric oxide release correlated with the mRNA data, which showed selective inhibition of LPS-mediated nitric oxide production. Although the regulatory mechanisms need to be further investigated, these results suggest that astrocyte-derived ${\beta}ig-h3$ may contribute to protection of the CNS from immune-mediated damage via controlling microglial inflammatory responses.

• 동의신경정신과학회지
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• 제19권2호
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• pp.95-110
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• 2008

Objective : This experiment was designed to investigate the effects of the PMCMT hot water extract & ultra-fine powder on Alzheimer's Disease Model Induced by ${\beta}A$. Method : The effects of the PMCMT hot water extract on expression of proinf1ammatory cytokine mRNA in BV2 microglial cell cell line treated by lipopolysacchaide(LPS). The effects of the PMCMT hot water extract & ultra-fine powder on (1) the behavior (2) AChE in serum (3) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. Result : 1. The PMCMT hot water extract suppressed the expression of proinflammatory cytokine mRNA in BV2 microglial cell line treated with LPS. 2. The PMCMT hot water extract & ultra-fine powder a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured stop-through latency and distance movement-through latency 3. The PMCMT hot water extract & ultra-fine powder suppressed the over-expression of AChE activity in the serum of the mice with Alzheimer's disease induced by ${\beta}A$. 5. The PMCMT ultra-fine powder reduced infarction area of hippocampus significantly, and the PMCMT hot water extract & ultra-fine powder controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. Conclusions : These results suggest that the PMCMT hot water extract & ultra-fine powder may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the PMCMT hot water extract & ultra-fine powder for Alzheimer's disease is suggested for future research.

• 대한본초학회지
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• 제23권3호
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• pp.73-83
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• 2008

Objectives : The root of Zingiber officinale ROSC. (Zingiberis Rhizoma Recens; Ginger) has been widely used as one of folk remedies and food materials in many traditional preparations. Ginger is known as an effective appetite enhancer and anti-inflammatory agent. This study was performed to investigate the effect of ginger chloroform fraction (GCF) in microglia which play a central role on brain inflammation in neurodegenerative diseases. Methods : Dried ginger was extracted with 80% methanol, and then fractionated with chloroform. BV2 mouse microglial cells were cultured with different concentrations of GCF and then stimulated with LPS (1 ${\mu}g/m{\ell}$) at indicated times. The cell toxicity of GCF was determined by MTT assay. The concentrations of NO, PGE2 and cytokines were measured by Griess assay and enzyme-linked immunosorbant assay. The mRNA and protein expressions of iNOS, COX-2 and cytokines were determined by RT-PCR and Western blotting. The phosphorylation of three MAPKs (p38 MAPK, ERK1/2 and JNK) and $NF-{\kappa}B$ activation were determined by Western blotting. Results : GCF significantly inhibited LPS-induced production of inflammatory mediators, NO, $PGE_2$ and proinflammatory cytokines ($TNF-{\alpha}$ and $IL-1{\beta}$) in a dose-dependent manner. GCF attenuated LPS-induced expression of mRNA and protein of inflammatory enzymes, iNOS, COX-2 and proinflammatory cytokines through suppressing the phosphorylation of ERK1/2 and p38 MAPK and the activation of p65 $NF-{\kappa}B$ in BV2 cells. Conclusions : This study suggests that GCF may have an anti-inflammatory property through suppressing the inflammatory mediator production released by activated microglia after the brain injury.