• 대한한의학방제학회지
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• 제8권1호
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• pp.257-279
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• 2000

Allergic contact dermatitis is a common skin disease resulting from specific immunologic to topically applied various allergen. After Dinitrochlorobenzene (DNCB) secondary sensitization, the ICR mice administered Rhemanniae radix extract (RRE) was observed to ascerstain the effect of RRE on allergic contact dermatitis. Purpose of this study was to investigate contact hypersensitivity assay, abdominal skin morphologic changes. Including mast cells and cell-surface glycoconjugates. The change of interleukin 2 (IL-2) receptor (CD25R). ICAM in abdominal skin, lymph node of inguinal region, and electro microscope-morphologic changes of abdominal skin. The results of this study were as follows: 1. The contact hypersensitivity assay, the ear swelling in the RRE had lesser probability than in the ACD Group. 2. In the general morphologic change of skin, hyperplasia of keratinocytes, distribution of vasculogenesis and epidermal lymphocytes infiltration were decreased in the RRE group compared with the ACD group. In epidermal basal layer and prickle layer, cell damage was decreased in the RRE group compared with the group painted with ACD. 3. MasT-cell in dermis was decreased in the RRE group compared with the group painted with DNCB. 4. Distribution of interlukin-2 Receptior positive cell and ICAM positive cell in dermis was decreased in the RRE Group compared with the ACD group. 5. Distribution of helper T-lymphocyte and cytotoxic T-lymphocite in inguinal nodes was decreased in the RRE group, and was observed well in paracortical area and cortical cord. 6. Distribution of apoptotic cell was appeared in the RRE group compared with the ACD group, in skin, dermis. in inguinal nodes, paracortical area observed well. With above results, the restarint of immunosuppression occuring in Allergic contact dermatitis is resulted in the slow progress the effect of Allergic contact dermatitis, and it is thought that ithis fact has a series of relation with apoptosis.

• 분석과학
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• 제31권6호
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• pp.232-239
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• 2018

Human breast milk (HBM) provides neonates with indispensable nutrition. The present study evaluated the anti-cancer activity of diluted and pasteurized early HBM (< 6 weeks' lactation) on human breast cancer cell lines. The cell lines MCF7 and MDA-MB231 were exposed to 1 % HBM from the 1st, 3rd, and 6th weeks of lactation and exhibited reduced proliferation rates. As controls, breast cell lines (293T and MCF-10A), breast cancer cell lines (MCF-7 and MDA-MB-231), and $CD133^{hi}CXCR4^{hi}ALDH1^{hi}$ patient-derived human cancer stem-like cells (KU-CSLCs) were treated with prominent milk proteins ${\beta}$-casein, ${\kappa}$-casein, and lactoferrin at varying doses (10, 50, and $100{\mu}g$) for 24 or 48 hrs. The impact of these proteins on cell proliferation was investigated. Breast cancer cell lines treated with ${\kappa}$-casein and lactoferrin exhibited significantly reduced viability, in both a dose- and time-dependent manner. Interestingly, ${\kappa}$-casein selectively impacted only cancer (but not normal breast) cell lines, particularly the more malignant cell line. However, ${\beta}$-casein-exposed human breast cancer cell lines exhibited a significantly higher proliferation rate. Thus, ${\kappa}$-casein and lactoferrin appear to exert selective anti-cancer activities. Further studies are warranted to determine the mechanisms underlying ${\kappa}$-casein- and lactoferrin-mediated cancer cell-selective cytotoxic effects.

• IMMUNE NETWORK
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• 제11권1호
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• pp.79-94
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• 2011

Background: Dendritic cell (DC)-based vaccines are currently being evaluated as a novel strategy for tumor vaccination and immunotherapy. However, inducing long-term regression in established tumor-implanted mice is difficult. Here, we show that deoxypohophyllotoxin (DPT) induces maturation and activation of bone marrow-derived DCs via Toll-like receptor (TLR) 4 activation of MAPK and NF-${\kappa}B$. Methods: The phenotypic and functional maturation of DPT-treated DCs was assessed by flow cytometric analysis and cytokine production, respectively. DPT-treated DCs was also used for mixed leukocyte reaction to evaluate T cell-priming capacity and for tumor regression against melanoma. Results: DPT promoted the activation of $CD8^+$ T cells and the Th1 immune response by inducing IL-12 production in DCs. In a B16F10 melanoma-implanted mouse model, we demonstrated that DPT-treated DCs (DPT-DCs) enhance immune priming and regression of an established tumor in vivo. Furthermore, migration of DPT-DCs to the draining lymph nodes was induced via CCR7 upregulation. Mice that received DPT-DCs displayed enhanced antitumor therapeutic efficacy, which was associated with increased IFN-${\gamma}$ production and induction of cytotoxic T lymphocyte activity. Conclusion: These findings strongly suggest that the adjuvant effect of DPT in DC vaccination is associated with the polarization of T effector cells toward a Th1 phenotype and provides a potential therapeutic antitumor immunity.

• 동의생리병리학회지
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• 제20권2호
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• pp.420-427
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• 2006

Immunological activities of the combined-administration of Ginseng Radix Rubra and Vitis Fructus were examined in C57BL/6 mice. Ginseng Radix Rubra and Vitis Fructus were extracted with distilled water or 40% ethyl alcohol. Ginseng Radix Rubra water extracts (GW), the mixture (1:1) of Ginseng Radix Rubra and Vitis Fructus water extracts [GVW(1:1)], the mixture (1:3) of Ginseng Radix Rubra and Vitis Fructus water extracts [GVW(1:3)], 40% ethyl alcohol extracts of Ginseng Radix Rubra (GE), the mixture (1:1) of Ginseng Radix Rubra and Vitis Fructus 40% ethyl alcohol extracts [GVE(1:1)] and the mixture (1:3) of Ginseng Radix Rubra and Vitis Fructus 40% ethyl alcohol extracts [GVE(1:3)] were administered p.o. once a day for 7 days, respectively. GVW(1:1) and GVW(1:3) decreased the viability of thymocytes increased by GW, but GVE(1:1) and GVE(1:3) increased the viability of thymocytes decreased by GE. GVW(1:1) and GVW(1:3) increased the viability of splenocytes decreased by GW or GE. Also, GVW(1:1) and GVE(1:1) enhanced the population of helper T cell in thymocytes, and GVE(1:1) and GVE(1:3) decreased the population of cytotoxic T cells increased by GE. Furthermore, GVW(1:1), GVW(1:3), GVE(1:1) and GVE(1:3) enhanced the population of $B220^+$ cells decreased by GW or GE, and decreased the population of $Thyl^+$ cells increased by GW or GE, and decreased the population of splenic $CD4^+$ cells increased by GW or GE. In addition, GVW(1:1) and GVW(1:3) decreased the phagocytic activity and the production of nitric oxide in peritoneal macrophages increased by GW, but GVE(1:1) and GVE(1:3) enhanced the phagocytic activity and the production of nitric oxide in peritoneal macrophages decreased by GE. These results suggest that Vitis Fructus has an regulative action on immune response of Ginseng Radix Rubra.

• 대한수의학회지
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• 제54권4호
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• pp.209-218
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• 2014

Experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS), reflects pathophysiologic steps in MS such as the influence of T cells and antibodies reactive to the myelin sheath, and the cytotoxic effect of cytokines. Galectin-9 (Gal-9) is a member of animal lectins that plays an essential role in various biological functions. The expression of Gal-9 is significantly enhanced in MS lesions; however, its role in autoimmune disease has not been fully elucidated. To identify the role of Gal-9 in EAE, we measured changes in mRNA and protein expression of Gal-9 as EAE progressed. Expression increased with disease progression, with a sharp rise occurring at its peak. Gal-9 immunoreactivity was mainly expressed in astrocytes and microglia of the central nervous system (CNS) and macrophages of spleen. Flow cytometric analysis revealed that $Gal-9^+CD11b^+$ cells were dramatically increased in the spleen at the peak of disease. Increased expression of tumor necrosis factor (TNF)-R1 and p-Jun N-terminal kinase (JNK) was observed in the CNS of EAE mice, suggesting that TNF-R1 and p-JNK might be key regulators contributing to the expression of Gal-9 during EAE. These results suggest that identification of the relationship between Gal-9 and EAE progression is critical for better understanding Gal-9 biology in autoimmune disease.