• 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.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.20 no.3
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• pp.71-81
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• 2007

Objective : In this study, herbal medicine(GJE, Gardenia jasminoides Ellis; HCT, Houttuynia cordata Thunb.; CIL, Chrysanthemum indicum Linne; PMS,Paeonia moutan Sims, P. subfruticosa Makino; APL, Agrimonia pilosa Ledebour) were screened for their inhibitory activities against Tyrosinase and PMA plus A23187-induced $TNF-{\alpha}$, IL-6, IL-8 productions in HMC-1 cells to reveal their skin -whitening and anti-allergic effect. Method : To investigate Tyrosinase inhibition we treated Mushroom Tyrosinase(Fluka, 93898) $10{\mu}{\ell}$ and 7.5mM Tyrosine (Sigma, T3754) $20{\mu}{\ell}$ with 80% ethanol medicine extracts. Then we observed 96well micro plate extinction at 490nm. In the next experiment, to investigate Anti-allergic effect we blended cultured Human Mast Cells(HMC-1) with medicine extracts. We treated the blended solution with Phorbol 12-myristate 13-acetate(PMA) and A23187, then observed $TNF-{\alpha}$, IL-6, IL-8 by ELISA (enzyme-linked immunosorbent assay) at 450nm. Results : In inhibiting Tyrosinase the results are as follows. 1. We observed 22% inhibition of Mushroom Tyrosinase at $500{\mu}g/m{\ell}$ concentration of GJE extracts. 2. We also could observe that the decreased Mushroom Tyrosinase activities in HCT, CIL extracts. In inhibiing $TNF-{\alpha}$, IL-6, IL-8 productions in HMC-1 cells the results are as follows. 1. Of the extracts examined, HCT, PMS, APL extracts showed over 50% inhibitions of Cytokines at $200{\mu}g/m{\ell}$ concentration. 2. In particular, APL extracts showed the best inhibitory effect on Cytokine productions in a dose-dependent manner. Conclusion : These results suggest that GJE extracts contributes to the anti melanin activities and represent a potential source of whitening agent. Thus these herbal medicines suggest novel drugs on anti-allergic effects.

• Nutritional Sciences
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• v.5 no.2
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• pp.60-67
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• 2002

Paeonia japonica var. pilosa $N_{AKAI}$, (PJ; Baek-Jak-Yak) is a medicinal plant which has been widely used as a component or blood-building decoctions. This study was performed to investigate the immunomodulative effects of PJ in mice, using in vitro and in vivo experiments. The immunomodulative effects were studied in vitro by determining the proliferation or mice splenocytes and the production of three kinds of cytokines (IL-1$\beta$, IL-6, TNF-$\alpha$) by mire peritoneal macrophages which were cultured with sequential fractions of PJ methanol extract (methanol, hexane, chloroform, ethylacetate, butanol and water). In an in vivo experiment using mice, different concentrations of PJ water extract were orally administrated every other day for two weeks. The production of cytokines (IL-1$\beta$, IL-6, TNF-$\alpha$) secreted by activated macrophages, and the proliferation of mice splenocytes, were used as indices for immunocompetence. In vitro supplementation using a hexane fraction of PJ in the range of 1 to 100 $\mu$ g/ml enhanced splenocyte proliferation by 1.8 to 12%, and by 10-15% using an aqueous fraction, compared to the control. IL-l$\beta$ production was significantly increased with the supplementation of butanol, hexane and water extracts of PJ Higher levels of IL-6 production were detected with supplementation of chloroform or water extracts. However, there were no significant differences in the production of TNF-$\alpha$ among the treated groups and the control. From the in vivo study, the highest proliferation of splenocytes was seen in the mice orally administrated with the PJ water extract at the concentration of 500 mg/kg body weight. In the case of cytosine production, IL-1-$\beta$, IL-6, and TNF-$\alpha$ released by activated peritoneal macrophages were augmented by the oral administration of a PJ water extract. These results indicate that Pl may enhance the immune function by regulating splenocyte proliferation and cytokine production capacity in mice.

• The Journal of Korean Obstetrics and Gynecology
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• v.22 no.2
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• pp.26-42
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• 2009

Purpose: This study was performed to evaluate the anti-inflammatory effect of Manbunbang extract (MBB). Methods: In order to understand the mechanism of anti-inflammatory effect of MBB, expression of cytokines and its levels in RAW 264.7 cell lines, as well as changes of cytokine gene expressions in serum, spleen, and liver tissues in acute inflammation induced mouse model were investigated. Results: 1. MBB significantly suppressed the expression levels of IL-1${\beta}$, TNF-${\alpha}$ and COX-2 mRNAs at 100 and 50 ${\mu}$g/m${\ell}$ concentrations, and IL-6 and NOS-II genes at 100, 50 and 10 ${\mu}$g/m${\ell}$ concentrations in RAW 264.7 cell lines, compared to those of the control. 2. MBB significantly reduced the production level of IL-$1{\beta}$, IL-6 and TNF-${\alpha}$ at 100 and 50 ${\mu}$g/m${\ell}$ concentrations in RAW 264.7 cell lines compared the those of the control. 3. MBB significantly reduced the production of IL-1${\beta}$, IL-6 and TNF-${\alpha}$ levels in sera of acute inflammation induced mice. 4. MBB significanlty suppressed the expression level of IL-1${\beta}$, TNF-${\alpha}$ mRNA in spleen tissues as well as IL-6 mRNA in liver tissues in acute inflammation induced mice. Conclusion: From the results above, anti-inflammatory effect of MBB through its immune regulation could be experimentally explained. Wide treatment of inflammatory diseases such as pelvic inflammation using MBB are recommended.

• Advances in Traditional Medicine
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• v.5 no.4
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• pp.251-261
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• 2005

Rheumatoid arthritis (RA) is an autoimmune/inflammatory disorder with a complex genetic component. RA is characterized by chronic inflammation of the synovial membrane in the joint, which leads to the progressive destruction of articular cartilage, ligament and bone. Several cytokines such as tumor necrosis $factor-{\alpha}\;TNF-{\alpha}\;and\;interleukin-1{\beta}\;(IL-1{\beta})$ and interleukin-6 (IL-6) have been implicated in the pathological mechanisms of synovial tissue proliferation, joint destruction and programmed cell death in rheumatoid joint. Genome wide screening of subjects suffering from autoimmune diseases especially arthritis revealed linkage to inflammatory molecules like $TNF-{\alpha},\;IL-1{\beta}$ and IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-kappaB $(NF-{\kappa}B)$ and human leucocyte antigen/major histocompatibility complex (HLA/MHC) locus. The status of the pharmacological mechanism of herbal drugs in the light of genome wide screening results has been discussed to reinforce the therapeutic potential and the pharmacological basis of the herbal drugs.

• Korean Journal of Veterinary Pathology
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• v.3 no.1
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• pp.15-25
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• 1999

To elucidate the mechanism of age-related development in FGS/NgaKIST mice with spontaneous glomerulosclerotic lesion, we examined expression and localization of various cytokine mRNA in the kidney in the progression of diseases. This mouse model is the first to develop spontanously occuring glomerosclerotic lesion in the kidney. In this study, we detected the up-regulation of local cytokine genes such as IL-1$\beta$, IL-2, IL-6, IL-10, TNF-$\alpha$, TGF-$\beta$, and IFN- $\gamma$ in the kidneys. In RT-PCR and Southern blot analysis, we detected gradual expressions of cytokine mRNA of IL-1$\beta$, IL-2, IL-6, IFN- $\gamma$, and TNF $\alpha$ mRNA during the course of disease. Other cytokines including IL -10 and TGF -$\beta$ were found to be appeared the slightly expressed level at 3 to 12 weeks before onset of inflammatory lesion but they are highly expressed at the end-stage of the disease accompaning high proteinurea and wasting. In situ RT-PCR, each cytokine mRNA were specifically localized in a variety of cells including mesangial, endothelial, parietal epithelial, tubular epithelial, arterial muscle cell, and infiltrated inflammatory cells. In addition, TNF - $\alpha$was detected moderately in the visceral and parietal epithelial cell, but weakly in endothelial and mesangial cells, whereas IL-1 $\beta$ and IL -6 were strong in mesangial regions. IL-6 and TNF- $\alpha$ was highly localized in the damaged proximal and collecting tubules. Especially, TGF -$\beta$ mRNA was highly found in mesangial cells within glomerulus and interstitium during the end-stage of this disease.. These results indicate that pro inflammatory cytokines such as IL-1 $\beta$, IL-2, IL-6, and TNF- $\alpha$ were gradually expressed from the early stage of this disease to the end-stage, and that IL-10 and TGF-$\beta$ may be important in the accumulation of extracellular matrix(ECM) within glomerulus and periglomerular fibrosis in the progression of this disease as well as tissue destruction in end-stage of this disease.

• Biomedical Science Letters
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• v.3 no.2
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• pp.139-150
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• 1997

In order to investigate the effect of aging and the $H_2O$$_2$ localization in association with histological, ultrastructural, and cytochemical studies in lung tissue after interleukin-1$\alpha$(IL-1) induced lung injury, an acute lung injury was induced by instillation of IL-1 into the trachea. Both of 4- and 20-months-old male rats, protein contents in IL-1 treated branchoalveolar lavage increased significantly compared to each control rats. Acute lung injury occured by oxidative stress because neutrophils accumulated in vascular lumen and formed the adhesion with endothelial cells. As these cause, tissue proteins were exuded and leukocytes migrated into the alveolar lumen. Neverthless in these lung injury $H_2O$$_2$ localization of IL-1 treated 20 months rats was not different compared to IL-1 treated 4 months rats. After all aging was not a factor to accelate IL-1 induced lung injury. Based on these results, it is suggested that neutrophil infilteration might be an important cause in acute lung injury, and aging is not a factor to change the acute lung injury by oxidative stress.

• Journal of Oriental Neuropsychiatry
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• v.18 no.3
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• pp.55-82
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• 2007

Ohjective: This research investigates the effect of the DJR on Alzheimer's disease. Method: 1.The effects of the DJR extract on IL.-$1{\beta}$, IL-6, TNF-${\alpha}$, cox-2, and NOS-II mRNA of BV2 microglia cell line treated with LPS; 2. the behavior: 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 DJR extract suppressed the expression of IL-$1{\beta}$, IL-6 and TNF-${\alpha}$ mRNA in BV2 microglia cell line treated with LPS. 2. The DJR extract suppressed the expression of IL-$1{\beta}$, IL-6, and TNF-${\alpha}$ protein production in BV2 microglia cell line treated with LPS. 3. For the DJR extract group a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by .${\beta}$A in the Moms water maze experiment, which measured stop-through latency, and distance movement-through latency. 4. The DJR extract suppressed the over-expression of IL-$1{\beta}$ protein, TNF-${\alpha}$ protein and CD68/CD11b, in the mice with Alzheimer's disease induced by ${\beta}$A 5. The DJR extract 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 DJR extract reduced the tau protein, GFAP protein, and presenilin1/2 protein (immunohistochemistry) of hippocampus in the mice with Alzheimer's disease induced by ${\beta}$A. Conclusion: These results suggest that the DJR extract may he effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the DJR extract for Alzheimer's disease of suggested for future research.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.1
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• pp.39-44
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• 2006

Type I diabetes (T1D) is an organ-specific autoimmune disease caused by the T cell-mediated destruction of the insulin-producing ${\beta}$ cells in the pancreatic islets. The onset of T1D is the consequence of a progressive destruction of islet ${\beta}$ cells mediated by an imbalance between effector $CD4^+$ T helper (Th)1 and regulatory $CD4^+$ Th2 cell function. Since interferon-alpha (IFN-${\alpha}$) has been known to modulate immune function and autoimmunity, we investigated whether administration of adenoviralmediated IFN-${\alpha}$ gene would inhibit the diabetic process in NOD mice. The development of diabetes was significantly inhibited by a single injection of adenoviral-mediated IFN-${\alpha}$ gene before 8 weeks of age. Next, we examined the hypothesis that Th2-type cytokines are associated with host protection against autoimmune diabetes, whereas Th1-type cytokines are associated with pathogenesis of T1D. The expression of IFN-${\alpha}$ induced increase of serum IL-4 and IL-6 (Th2 cytokines) levels and decrease of serum IL-12 and IFN-${\gamma}$ (Th1 cytokines) levels. Therefore, overexpression of IFN-${\alpha}$ by adenoviralmediated delivery provides modulation of pathogenic progression and protection of NOD mice from T1D.