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41 results on '"Kim, Min-Jong"'

19. A Study on the Actual Condition and Development Plan of Psychological Warfare in NORTH KOREA

Author

Kim Dae eun, Shim Jin sub, Kim Min jong, and Song Kyung jae

Subjects
Development plan, Politics, Political science, Political economy, Psychological Warfare, Sacrifice, Absolute advantage
Abstract

Psychological Warfare against NORTH KOREA with an absolute advantage from NORTH KOREA was sus-pended as it was used as a role of political sacrifice...

Published
2017

23. Gomisin M2 Inhibits Mast Cell-Mediated Allergic Inflammation via Attenuation of FcεRI-Mediated Lyn and Fyn Activation and Intracellular Calcium Levels

Author

Dhakal, Hima, primary, Lee, Soyoung, additional, Kim, Eun-Nam, additional, Choi, Jin Kyeong, additional, Kim, Min-Jong, additional, Kang, Jinjoo, additional, Choi, Young-Ae, additional, Baek, Moon-Chang, additional, Lee, Byungheon, additional, Lee, Hyun-Shik, additional, Shin, Tae-Yong, additional, Jeong, Gil-Saeng, additional, and Kim, Sang-Hyun, additional

Published
2019
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30. Ethanol Extract of Ampelopsis brevipedunculata Rhizomes Suppresses IgE-Mediated Mast Cell Activation and Anaphylaxis

Author

Park, Ji-Yeong, Kim, Min-Jong, Choi, Young-Ae, Woong Lee, Seung, Lee, Soyoung, Hyun Jang, Yong, and Kim, Sang-Hyun

Abstract

More than 20% of the world’s population suffers from allergic diseases, including allergic asthma, rhinitis, and atopic dermatitis that severely reduce the patient’s quality of life. The treatment of allergy has been developed, but there are still unmet needs. Ampelopsis brevipedunculata (Maxim.) Trautv. is a traditional medicinal herb with beneficial bioactivities, such as antioxidant, anti-hypertension, anti-viral, anti-mutagenic, and skin and liver (anti-hepatotoxic) protective actions. However, its anti-allergic effect has not been addressed. This study designed to investigate the pharmacological effect of an ethanol extract of A. brevipedunculata rhizomes (ABE) on mast cell and anaphylaxis models. For in vivo studies, we used ovalbumin-induced active systemic anaphylaxis (ASA) and immunoglobulin (Ig) E-mediated passive cutaneous anaphylaxis (PCA) models. In ASA model, oral administration of ABE (1, 10, and 100 mg/kg) attenuated the anaphylactic responses, such as hypothermia, serum histamine, and IgE productions. In PCA model, ABE also suppressed the plasma extravasation and swelling. The underlying mechanisms of action were identified in various mast cell types. In vitro, ABE (10, 30, and 60 µg/mL) inhibited the release of essential allergic mediators, such as histamine and β-hexosaminidase, in a concentration-dependent manner. ABE prevented the rapid increase in intracellular calcium levels induced by the DNP-HSA challenge. In addition, ABE downregulated the tumor necrosis factor-α and interleukin-4 by suppressing the activation of nuclear factor-κB. Collectively, this study is the first to identify the anti-allergic effect of ABE, suggesting that ABE is a promising candidate for treating allergic diseases.

Published
2024
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31. SG-SP1 Suppresses Mast Cell-Mediated Allergic Inflammation via Inhibition of FcεRI Signaling.

Author

Kim, Min-Jong, Je, In-Gyu, Song, Jaeyoung, Fei, Xiang, Lee, Soyoung, Yang, Huiseon, Kang, Wonku, Jang, Yong Hyun, Seo, Seung-Yong, and Kim, Sang-Hyun

Subjects
ANTIALLERGIC agents, MAST cell disease, MAST cells, SURFACE plasmon resonance, GALLIC acid, INTRACELLULAR calcium, EPIGALLOCATECHIN gallate
Abstract

Background: As the number of allergic disease increases, studies to identify new treatments take on new urgency. Epigallocatechin gallate (EGCG), a major component of green tea, has been shown to possess a wide range of pharmacological properties, including anti-inflammation and anti-viral infection. In previous study, gallic acid (GA), a part of EGCG, has shown anti-allergic inflammatory effect. To improve on preliminary evidence that GA has allergy mitigating effect, we designed SG-SP1 based on GA, and aimed to assess the effects of SG-SP1 on mast cell-mediated allergic inflammation using various animal and in vitro models. Methods: For in vitro experiments, various types of IgE-stimulated mast cells (RBL-2H3: mast cell-like basophilic leukemia cells, and primary cultured peritoneal and bone marrow-derived mast cells) were used to determine the role of SG-SP1 (0.1–1 nM). Immunoglobulin (Ig) E-induced passive cutaneous anaphylaxis and ovalbumin-induced systemic anaphylaxis, standard animal models for immediate-type hypersensitivity were also used. Results: For in vitro , SG-SP1 reduced degranulation of mast cells by down-regulating intracellular calcium levels in a concentration-dependent manner. SG-SP1 decreased expression and secretion of inflammatory cytokines in activated mast cells. This suppressive effect was associated with inhibition of the phosphorylation of Lyn, Syk and Akt, and the nuclear translocation of nuclear factor-κB. Due to the strong inhibitory effect of SG-SP1 on Lyn, the known upstream signaling to FcεRI-dependent pathway, we confirmed the direct binding of SG-SP1 to FcεRI, a high affinity IgE receptor by surface plasmon resonance experiment. Oral administration of SG-SP1 hindered allergic symptoms of both anaphylaxis models evidenced by reduction of hypothermia, serum IgE, ear thickness, and tissue pigmentation. This inhibition was mediated by the reductions in serum histamine and interleukin-4. Conclusions: We determined that SG-SP1 directly interacts with FcεRI and propose SG-SP1 as a therapeutic candidate for mast cell-mediated allergic inflammatory disorders via inhibition of FcεRI signaling. [ABSTRACT FROM AUTHOR]

Published
2020
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32. Elaeocarpusin Inhibits Mast Cell-Mediated Allergic Inflammation

Author

Kim, Min-Jong, primary, Kim, Yeon-Yong, additional, Choi, Young-Ae, additional, Baek, Moon-Chang, additional, Lee, Byungheon, additional, Park, Pil-Hoon, additional, Shin, Tae-Yong, additional, Kwon, Taeg Kyu, additional, Khang, Dongwoo, additional, and Kim, Sang-Hyun, additional

Published
2018
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35. 2-Hydroxy-3-methoxybenzoic acid attenuates mast cell-mediated allergic reaction in mice via modulation of the FcεRI signaling pathway

Author

Kim, Yeon-Yong, primary, Je, In-Gyu, additional, Kim, Min Jong, additional, Kang, Byeong-Cheol, additional, Choi, Young-Ae, additional, Baek, Moon-Chang, additional, Lee, Byungheon, additional, Choi, Jin Kyeong, additional, Park, Hae Ran, additional, Shin, Tae-Yong, additional, Lee, Soyoung, additional, Yoon, Seung-Bin, additional, Lee, Sang-Rae, additional, Khang, Dongwoo, additional, and Kim, Sang-Hyun, additional

Published
2016
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36. 2-Hydroxy-3-methoxybenzoic acid attenuates mast cell-mediated allergic reaction in mice via modulation of the FcεRI signaling pathway

Author

Kim, Yeon-Yong, Je, In-Gyu, Kim, Min Jong, Kang, Byeong-Cheol, Choi, Young-Ae, Baek, Moon-Chang, Lee, Byungheon, Choi, Jin Kyeong, Park, Hae Ran, Shin, Tae-Yong, Lee, Soyoung, Yoon, Seung-Bin, Lee, Sang-Rae, Khang, Dongwoo, and Kim, Sang-Hyun

Abstract

Mast cells are important effector cells in immunoglobulin (Ig) E-mediated allergic reactions such as asthma, atopic dermatitis and rhinitis. Vanillic acid, a natural product, has shown anti-oxidant and anti-inflammatory activities. In the present study, we investigated the anti-allergic inflammatory effects of ortho-vanillic acid (2-hydroxy-3-methoxybenzoic acid, o-VA) that was a derivative of vanillic acid isolated from Amomum xanthioides. In mouse anaphylaxis models, oral administration of o-VA (2, 10, 50 mg/kg) dose-dependently attenuated ovalbumin-induced active systemic anaphylaxis and IgE-mediated cutaneous allergic reactions such as hypothermia, histamine release, IgE production and vasodilation; administration of o-VA also suppressed the mast cell degranulator compound 48/80-induced anaphylaxis. In cultured mast cell line RBL-2H3 and isolated rat peritoneal mast cells in vitro, pretreatment with o-VA (1–100 μmol/L) dose-dependently inhibited DNP-HSA-induced degranulation of mast cells by decreasing the intracellular free calcium level, and suppressed the expression of pro-inflammatory cytokines TNF-α and IL-4. Pretreatment of RBL-2H3 cells with o-VA suppressed DNP-HSA-induced phosphorylation of Lyn, Syk, Akt, and the nuclear translocation of nuclear factor-κB. In conclusion, o-VA suppresses the mast cell-mediated allergic inflammatory response by blocking the signaling pathways downstream of high affinity IgE receptor (FcεRI) on the surface of mast cells.

Published
2017
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39. Loss of ARID1 A expression is associated with poor prognosis in small intestinal carcinoma.

Author

Kim, Min Jong, Gu, Mi Jin, Chang, Hee‐Kyung, and Yu, Eunsil

Subjects
*ADENOSINE triphosphate, *SMALL intestine diseases, *IMMUNOCHEMISTRY, *SIGNET rings, *MULTIPLE regression analysis, *CARCINOMA
Abstract

Aims To investigate AT-rich interactive domain-containing protein 1A ( ARID1A) and p53 expression in small intestinal carcinoma ( SIC) and to determine its prognostic significance. Methods and results Immunohistochemical staining for ARID1A and p53 was performed in 178 SICs using a tissue microarray (TMA). Loss of or low ARID1A expression was observed in 36 (20.2%) and 60 (33.7%) of cases, respectively. Aberrant p53 expression was observed in 99 (55.6%) cases. Loss of or low ARID1A expression was found to be associated with signet ring cell carcinoma and undifferentiated carcinoma, a high-grade tumour, and a higher T stage. No relationship was found between aberrant p53 expression and clinicopathological factors or overall survival. Patients with loss of ARID1A expression, irrespective of p53 expressional status, showed significantly poorer overall survival than those expressing ARID1A. Multiple regression analysis revealed that grade and pT stage were associated significantly with ARID1A loss, and multivariate analysis showed that patients with high ARID1A expression had a lower risk of death than those with loss of ARID1A expression. Conclusions Low or loss of ARID1A expression is correlated significantly with a high-grade tumour, higher T stage, and poorer overall survival. These findings suggest that ARID1A expression could be used as a prognostic marker in SIC. [ABSTRACT FROM AUTHOR]

Published
2015
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