• The Journal of Korean Medicine
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• v.28 no.2 s.70
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• pp.137-154
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• 2007

Objective : This experiment was designed to investigate the effect of the GYZB hot water extract & ultra-fine powder on the Alzheimer's disease model induced by amyloid ${\beta}$ protein (${\beta}A$). Method : We measured the effects of the GYZB hot water extract on expression of $IL-1{\beta}$, IL-6 mRNA and production of IL-6, $TNF-{\alpha}$ in the BV2 microglial cell line treated with lipopolysaccharide (LPS). The effects of the GYZB hot water extract & ultra-fine powder on (1) the behavior, (2) expression of $IL-1{\beta}$ and $TNF-{\alpha}$, (3) glucose in serum, (4) the infarction area of the hippocampus, and brain tissue injury in mice induced with Alzheimer's diseased by ${\beta}A$ were investigated. Results : The GYZB hot water extract suppressed the expression of $IL-1{\beta}$ and IL-6 mRNA and significantly suppressed the production of IL-6 and $TNF-{\alpha}$ in the BV2 microglial cell line treated with LPS. The GYZB hot water extract & ultra-fine powder showed a significant inhibitory effect on the memory deficit of 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. The GYZB ultra-fine powder significantly suppressed the expression of $IL-1{\beta}$ and $TNF-{\alpha}$ protein, and the GYZB hot water extract significantly suppressed the expression of $TNF-{\alpha}$ protein in the microglial cell of mice with Alzheimer's disease induced by ${\beta}A$. The GYZB hot water extract & ultra-fine powder reduced the infarction area of hippocampus in the mice with Alzheimer's disease induced by ${\beta}A$. Conclusions : These results suggest that GYZB hot water extract & ultra-fine powder may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of GYZB for Alzheimer's disease is suggested for future research.

• The Journal of Pediatrics of Korean Medicine
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• v.19 no.2
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• pp.175-195
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• 2005

Objective: This experimental study was performed to examine the in vitro and in viva anti-inflammatory and anti-allergic effects of Mori Cortex. Methods: Water extract of Mori Cortex was studied to its ability to stimulate or inhibit macrophage 264.7 cells to produce inflammatory and allergic mediators. Cytokines such as $IL-1{\beta}$, IL-6, IL-10 and $TNF-{\alpha}$ were measured by immunochemical assay. In vitro, the macrophages 264.7 were classified into four groups. One group was a normal group. The other group was a (-) control group stimulated with LPS. And the third group was a (+) control group pretreated for 1 hour with hydrocortisone. And the fourth group was a sample group pretreated for 1 hour with Mori Cortex. After pretreatment, macrophage were incubated with lipopolysaccharide(LPS) $100\;ng/m{\ell}$ for 12 hour and media collected and $IL-1{\beta}$, IL-6, IL-10 and $TNF-{\alpha}$ concentrations in supernatants were measured each by Enzyme linked immuno-soubent assay. Mori Cortex were used $50\;{\mu}g/m{\ell},\;100\;{\mu}g/m{\ell},\;250\;{\mu}g/m{\ell},\;500\;{\mu}g/m{\ell},\;and\;1,000\;{\mu}g/m{\ell}$. Hydrocortisones were used $10^{-8}M,\;10^{-7}M,\;10^{-6}M,\;10^{-5}M\;and\;10^{-4}M$. In vivo, the SD rats were classified into three groups. One group was a normal group injected with normal saline into the abdominal cavity. The other was a control group prescribed to compound 48/80 after normal saline injection. And the third was a sample group prescribed to compound 40/80 after Mori Cortex injection. Then, the release of histamine, IL-6 and $TNF-{\alpha}$ were measured. Results : In vitro, Man Cortex significantly increased the release of $IL-1{\beta}\;and\;TNF-{\alpha}$ by LPS-stimulated macrophage 264.7 cells. And it significantly decreased the release of IL-10. In IL-6, Mori Cortex of low concentration significantly decreased the release of IL-6, but that of high concentration acted in reverse. In vivo, Man Cortex didn't show significant inhibitory effects on the release of histamine and IL-6 in comparison with that of the control group. But it significantly increased the release of $TNF-{\alpha}$ in comparison with that of the control group.

• IMMUNE NETWORK
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• v.5 no.1
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• pp.30-35
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• 2005

Background: p38 and extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) signaling are thought to have critical role in lipopolysaccharide (LPS)-induced immune response but the molecular mechanism underlying the induction of these signaling are not clear. Methods: Specific inhibitors for p38, SB203580, and for ERK, PD98059 were used. Cells were stimulated by LPS with or without specific MAPK inhibitors. Results: LPS activated inducible nitric oxide synthase (iNOS), subsequent NO productions, and pro-inflammatory cytokine gene expressions (TNF-${\alpha}$, IL-$1{\beta}$, IL-6, and IL-12). Treatment of both SB203580 and PD98059 decreased LPS-induced NO productions. Concomitant decreases in the expression of iNOS mRNA and protein were detected. SB203580 and PD98059 decreased LPS-induced gene expression of IL-$1{\beta}$ and IL-6. SB203580 increased LPS-induced expression of TNF-${\alpha}$ and IL-12, and reactive oxygen species production, but PD98059 had no effect. Conclusion: These results indicate that both p38 and ERK pathways are involved in LPS-stimulated NO synthesis, and expression of IL-$1{\beta}$ and IL-6. p38 signaling pathways are involved in LPS-induced TNF-${\alpha}$ and IL-12, and reactive oxygen species plays an important role in these signaling in macrophage.

• Journal of Applied Biological Chemistry
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• v.55 no.4
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• pp.221-225
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• 2012

The anti-inflammatory effects of Undaria pinnatifida water extract (UPWE) were investigated using lipopolysaccharide-induced inflammatory response in this study. To examine the potential anti-inflammatory properties of UPWE, the cell proliferation, nitric oxide (NO), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-${\alpha}$) and IL-$1{\beta}$ were measured. As a result, there was no cytotoxicity in the macrophage proliferation treated with UPWE compared to the control. NO levels decreased with increasing concentration of UPWE. Moreover, the secretion of IL-6, TNF-${\alpha}$ and IL-$1{\beta}$ were suppressed in a dose-dependent manner, and IL-6 inhibition activities were over 50% at 0.1%. These results suggested that UPWE may have significant effects on inflammatory factors and be a potential anti-inflammatory therapeutic materials.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.4
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• pp.929-935
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• 2006

This study was to investigate the effect of Danchunwhangagam(DCWGG) extract on the production of proinflammatory cytokines in peripheral mononuclear cells (PBMCS) from Cerebral infarction(CI) patients. Methods: We examined that the inhibition rate of tumor necrosis factor $(TNF)-{\alpha},\;interleukin(IL)-1{\alpha},\;IL-1{\beta}$, IL-6, and IL-8 productions in DCWGG pretreatment PBMCs culture supernatant in the lipopolysaccaride(LPS)- or Oesferrioxamine(DFX)-treated cells compared to unstimulated cells. DCWGG inhibited the productions of $TNF-{\alpha},\;IL-1{\alpha},\;IL-1{\beta}$, IL-6, and IL-8 induced by LPS in a dose-dependent manner DCWGG might have regulatory effects on LPS or DFX-induced cytokine production, which might explain its beneficial effect in the treatment of CI.

• Korean Journal of Pharmacognosy
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• v.42 no.3
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• pp.253-259
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• 2011

Macrophages play a vital role in the innate immune system involving defensive cytokines such as TNF (tumor necrosis factor)-${\alpha}$ and nitric oxide (NO). Therefore, we try to elucidate the anti-inflammatory activity of Chaga mushroom (Inonotus Obliquus, IO) in murine macrophages. Raw 264.7 cells and peritoneal macrophages of mice were cultured with or without LPS/LPS + IFN-${\gamma}$ in the presence of IO aqueous extracts (IOE 0.2, 2, 20, 100 ${\mu}g$/mL) for 24 hr and 48 hr, respectively. Exposure of IOE caused the decrease of NO production and increase of TNF-${\alpha}$ production in dose-dependent manner in activated peritoneal macrophage in vitro. To further investigate anti-inflammatory effects of IO ex vivo, we orally administrated capsaicin (PC, 3 mg/kg/day) and IOE (100, 200, 400 mg/kg/day) for 4 consecutive days to C57BL/6 mice (7~9 weeks old, female), then observed the NO secretion and cytokine (TNF-${\alpha}$) production of LPS/LPS + INF-${\gamma}$-stimulated peritoneal macrophages. IOE inhibits NO secretion in dose-dependent manner both ex vivo and in vitro and increases the production of TNF-${\alpha}$ in vitro. In addition, we found that IOE possessed suppressive effects of LPS-stimulated TNF-${\alpha}$, IL-$1{\beta}$, COX-2, as well as iNOS expressions in Raw 264.7 cells. These findings indicate that IOE suppress not only the LPS-induced NO overproduction of murine peritoneal macrophages, but also iNOS, COX-2, TNF-${\alpha}$, and IL-$1{\beta}$ overexpression of LPS-induced Raw 264.7 cells. Consequently, our results suggest that IO may have the anti-inflammatory effects via suppression of the inflammatory cytokines and mediators, and be useful for the treatment of inflammatory diseases.

• Biomedical Science Letters
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• v.10 no.2
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• pp.65-73
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• 2004

I report that single-stranded antisense as a part of large circular (LC-) genomic DNA of recombinant M13 phage exhibits enhanced stability, sequence specific antisense activity, and no need for target site search. A cDNA fragment (708 bp) of rat TNF-$\alpha$ was inserted into a phagemid vector, and TNF-$\alpha$ antisense molecules (TNF$\alpha$-LCAS) were produced as single-stranded circular DNA. When introduced into a rat monocyte/macrophage cell line, WRT7/P2, TNF$\alpha$-LCAS was able to ablate LPS-induced TNF-$\alpha$ mRNA to completion. The antisense effect of TNF$\alpha$-LCAS was shown to be sequence-specific because expressions of three control genes ($\beta$-actin, GAPDH and IL-1$\beta$) were not significantly altered by the antisense treatment. Further, TNF$\alpha$-LCAS was found to be highly efficacious as only 0.1 $\mu$g (0.24 nM) of TNF$\alpha$-LCAS was sufficient to block TNF-$\alpha$ expression in 1$\times10^5$ WRT7/P2 cells. I have also observed specific antisense activity in reduction of NF-$\kappa$B gene expression. The results suggest that an antisense sequence as a part of single-stranded circular genomic DNA has a specific antisense activity.

• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.6
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• pp.915-921
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• 2012

Artemisiae Asiaticae Herba (AAH) has been used to remedy of symptoms such as bleeding, dysmenorrhea, eczema and itchy skin in Oriental Medicine. In this study, we investigated the protective effect of AAH on allergic response. The effect of AAH was analyzed by ELISA and RT-PCR in RBL-2H3 cells. We investigated cell viability, ${\beta}$-hexosaminidase and histamine as markers of degranulation, production of IL-4 and TNF-${\alpha}$, and gene expression of HDC2, cytokines and $Fc{\varepsilon}RI$ ${\alpha}{\beta}{\gamma}$ subunit. We found that AAH suppressed ${\beta}$-hexosaminidase and histamine release, the production of IL-4 and TNF-${\alpha}$ in RBL-2H3 by the anti-DNP IgE plus DNP-HSA stimulation. AAH also significantly decreased cytokine mRNA expressions, such as IL-$1{\beta}$, IL-2, IL-3, IL-4, IL-5, IL-6, IL-12, IL-13, TNF-${\alpha}$, and GM-CSF, and increased cytokine mRNA expressions of IL-10 in RBL-2H3. In addition, AAH suppressed mRNA expression of $Fc{\varepsilon}RI$ ${\alpha}{\beta}{\gamma}$ subunit on cell surface. Our results indicate that AAH protects against allergic response and exerts an anti-inflammatory effect through the inhibition of degranulation and production of cytokines and expression of $Fc{\varepsilon}RI$ ${\alpha}{\beta}{\gamma}$ subunit.

• Journal of Oriental Neuropsychiatry
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• v.19 no.3
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• pp.85-100
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• 2008

Objective: This experiment was designed to investigate the effect of the KSKH hot water extract & ultra-fine powder on microglia and memory deficit model. Method: The effects of the KSKH hot water extract on expression of IL-1$\beta$, IL-6, TNF-$\alpha$ mRNA and production of IL-1$\beta$, IL-6, TNF-$\alpha$ in BV2 microglial cell line treated by lipopolysacchaide(LPS) were investigated. The effects of the KSKH hot water extract & ultra-fine-fine powder on the behavior of the memory deficit mice induced by scopolamine and AChE in serum of the memory deficit mice induced by scopolamine were investigated. Results: 1. The KSKH hot water extract suppressed the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ mRNA in BV2 microglial cell line treated by LPS. 2. The KSKH hot water extract suppressed the production of IL-1$\beta$, IL-6, TNF-$\alpha$ in 100$\mu g/m\ell$ concentration of BV2 microglial cell line culture supernatant. 3. The KSKH hot water extract & ultra-fine powder decreased AChE activation significantly in the serum of the memory deficit mice induced by scopolamine. 4. The KSKH hot water extract & ultra-fine powder showed significant effect on memory impairment in the stop-through latency type of Morris water maze test. Conclusions: This experiment shows that the KSKH hot water extract & ultra-fine powder might be effective for the prevention and treatment of amnesia and Alzheimer's disease. Investigation into the clinical use of the KSKH hot water extract & ultra-fine powder for amnesia and Alzheimer's disease is suggested for future research.

• Korean Journal of Oriental Medicine
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• v.11 no.2
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• pp.97-111
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• 2005

This study was performed to evaluate anti-thrombotic activities and anti-inflammatory effects of ChungyeolHaedogHwaeoTang water extract(CHHT). The results were summarized as follows. In experiment of anti-thrombotic effect; 1. CHHT inhibited human platelet aggregation induced by ADP and epinephrine as compared with the control group, and inhibited pulmonary embolism induced by collagen and epinephrine (inhibitory rate is 37.5%). 2. CHHT increased platelet number significantly, and also CHHT shortened PT and APTT significantly as compared with the control group in thrombus model induced by dextran. In experiment of anti-inflammatory effect; 3. CHHT inhibited $IL-1{\beta}$, IL-6, TNF-${\alpha}$, COX-2 and NOS-II mRNA expression as compared with the control group in a concentration-dependent degree, and inhibited NO production significantly at 50, 100 ${\mu}g/ml$, and also inhibited ROS production in a concentration-dependent degree as compared with the control of group in RAW 264.7 cell line. 4. CHHT inhibited $IL-1{\beta}$, IL-6 and TNF-${\alpha}$ production significantly in serum of acute inflammation-induced mice, and decreased $IL-1{\beta}$, IL-6 and TNF-${\alpha}$ production in spleen tissue, and also decreased $IL-1{\beta}$, and IL-6 production in liver tissue, but increased TNF-${\alpha}$ production in liver tissue of acute inflammation-induced Balb/c mice. 5. CHHT increased survival rate from the 3rd day in ICR mice with lethal endotoxemia induced by LPS. These results suggest that CHHT can be useful in treating diverse female diseases caused by thrombosis and inflammation such as menstrual pain, menstrual disorder, leukorrhea, vaginitis, cervicitis, pelvic inflammatory disease and so on.