• 대한의생명과학회지
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• 제16권3호
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• pp.179-185
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• 2010

Benzene is known as a ubiquitous air pollutant and has a carcinogenic influence on the human body. Benzene is also metabolized to other volatile organic compounds (VOCs) in the body such as phenol and hydroquinone (HQ). The metabolites are accumulated and further oxidized by myeloperoxidase in bone marrow. They act as toxic agents and cause a variety of diseases, including cancer, atopic dermatitis and asthma. In this study, we examined the effects of benzene and its metabolites on proliferation, differentiation and chemotaxis of EoL-1 cells, the human eosinophilic leukemia cell line. These chemicals had no effect on the proliferation of EoL-1 cells. Benzene decreased the differentiation of EoL-1 cells induced by butyric acid. HQ was induced the cell death during butyric acid-induced EoL-1 cell differentiation. In a chemotaxis experiment, benzene, phenol and HQ enhanced the cell migration induced by Lkn-1 but not by MCP-1, eotaxin, MIP-$1{\alpha}$ and RANTES. These findings provide the effect of VOCs on the regulation of eosinophil-involved immune response.

• 혜화의학회지
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• 제18권2호
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• pp.47-62
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• 2009

Atopic dermatitis induced NC/Nga mice were used to investigate the efficacy of HYT on the recovery of dermatitic symptoms by how HYT influenced the immune related factors. The results are as below: 1. Compared to the control, HYT treated group showed recovery of atopic dermatitis by the naked eye observation, and significant reduction of dermatits index was observed after 14 weeks. 2. HYT treated group showed significant decrease of the ratio of CCR3+, B220+/IgE+, and Gr-1+/CD11b+ immune cells in dorsal skin by 40.5%, 34.2%, and 48.1%, respectively. 3. HYT treated group showed increase in the ratio of CD19+ immune cells within PBMC by 10.8%, as well as decrease in CD3+, CD3+/CD69+, NKT+ ratios by 5.3%, 35.2%, and 44.9%, respectively. 4. HYT treated group showed increase in the expression of IFN-$\gamma$ in serum by 589.3%, whereas the expression of IL-4, IL-5, IL-6, IL-13, TNF-$\alpha$, MCP-1 and RANTES were decreased by 31.4%, 82.1%, 97.1%, 39.5%, 83.7%, 26.1%, 48.6%, respectively. A 47.2% decrease in IgE expression was also observed. The results above strongly supported the improvement of atopic dermatitis by HYT treatment through immune modulation. Further studies on the synergistic effect of each ingredients of HYT and therapeutic effects according to the dosage of each ingredient should be followed for clinical applications. This work was (partly) supported by the RIC program of MKE(Ministry of Knowledge Economy) in Daejeon University.

• 혜화의학회지
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• 제18권2호
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• pp.63-79
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• 2009

Atopic dermatitis induced NC/Nga mice were used to investigate the efficacy of Hyunggaeyunkyotanggamibang(HYGB) on the recovery of dermatitic symptoms through its influence on the immune related factors. The results are as below: 1. HYGB treated group showed improvement of atopic dermatitis with naked eye observation, and significant decrease of dermatitis index was observed after 14 weeks. 2. HYGB treated group showed significant decrease of the ratio of CCR3+, B220+/IgE+, and CD11b+/Gr-1+ immune cells in dorsal skin by 41.7%, 21.5%, and 23.8%, respectively. 3. HYGB treated group showed an increase of CD19+ immune cells by 10.3% in PBMC, whereas CD3+, CD3+/CD69+, NKT+ immune cells were decreased by 4.3%, 42.9%, and 21.7%, respectively. 4. HYGB treated group showed an increase in the expression of IFN-$\gamma$ in the serum by 514.3%. However, the expressions of IL-4, IL-5, IL-6, IL-13, TNF-$\alpha$, MCP-1 and RANTES were decreased by 21.2%, 69.8%, 90.5%, 28.7%, 72.2%, 26.1%, and 19.9%, respectively. Also, the expression of IgE was decreased by 44.3%. 5. HYGB treated group showed a decrease of the expression of IL-4 and IL-5 by 43% and 44.3%. The results above indicated that HYGB clinically used for atopic dermatitis treatment has objective validity, and therefore can be provided as the basic data for EBM(Evidence based medicine) construction for anti-allergic and anti-inflammatory studies.

• BMB Reports
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• 제44권4호
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• pp.273-278
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• 2011

Destruction of the skin barrier by thermal injury induces microbial invasion, which can lead to the development of systemic infection and septic shock. Microbial pathogens possess pathogen-associated molecular patterns (PAMPs), which are recognized by conserved receptors. To understand the role of PAMPs in thermal injury-induced mice, LPS or CpG-DNA were topically applied to dorsal skin after thermal injury. We observed an increase in the number of inflammatory cell infiltrates as well as thickening in the dermis upon treatment with LPS or CpG-DNA. We also found that expression of IL-$1{\beta}$, MIP-2, and RANTES induced by thermal injury was enhanced by LPS or CpG-DNA. In addition, the proportions of $CD4^+$ and $CD^8+$ T cells in the spleen and lymph nodes were altered by LPS or CpG-DNA. These results provide important information concerning PAMPs-induced inflammation upon thermal injury and provide a basis for studying the role of PAMPs in thermal injury-induced complications.

• 대한한방부인과학회지
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• 제27권2호
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• pp.1-11
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• 2014

Objectives: The purpose of this study was to investigate the effects of Longanae Arillus water extract (LA) on the production of inflammatory mediators in RAW 264.7 cell. LA is used for forgetfulness, insomnia, palpitation symptoms in korean medicine. Methods: In order to evaluate cytotoxicity of LA, cell viability was measured. To investigate anti-inflammatory effects of LA in the lipopolysacharide (LPS)-induced RAW 264.7 cell, the concentration of nitric oxide (NO) and cytokines were measured. And when p-value is below 0.05, it is judged to have the significant difference statistically. Results: 1. LA showed no cytotoxicity. 2. LA inhibited significantly the production on NO at the concentration of 50 and $200{\mu}g/ml$. 3. LA inhibited significantly the production on interleukin (IL)-$1{\beta}$ at the concentration of 25, 50, 100 and $200{\mu}g/ml$. 4. LA inhibited significantly the production on tumor necrosis factor (TNF)-${\alpha}$ at the concentration of 50, 100 and $200{\mu}g/ml$. 5. LA inhibited significantly the production on lipopolysaccharide-induced chemokine (LIX) at the concentration of 25, 100 and $200{\mu}g/ml$. 6. LA inhibited significantly the production on regulated on activation normal T cell expressed and secreted (RANTES) at the concentration of $200{\mu}g/ml$. Conclusions: These results suggest that LA has anti-inflammatory effect.

• Journal of Acupuncture Research
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• 제20권4호
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• pp.53-65
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• 2003

Although the effect of Bee Venom has been reported, its mechanism has not been fully elucidated. Nitric Oxide(NO) is one of the free radicals and mediates in inflammation diseases. Chemokines contribute to the pathogenesis of several disorders such as allergic rhinitis and rheumatoid arthritis and so on. The objective of this study was to investigate the scavenging effect of Bee Venom on NO and on expression of chemokine genes. There was no significant NO scavenging effect in Crude Bee Venom, Apamin, Melittin, and MCD-peptide. The expression of chemokines was examined by RT-PCR using the human mast cell line(HMC-1), which is known to secrete and express chemokines. In order to investigate the protective effect of Bee Venom, HMC-1 cells were incubated with pretreatment of Bee Venom for 24 hrs and stimulated with 1 uM calcium ionophore A23178 for 2 hrs. RT-PCR analyses of chemokine genes showed that expressions of RANTES and MCP-1 were increased compared to the calcium ionophore-only treated group. But IL-8 and MCP-3 did not express increasing effect compared to control group. This study may provide important basic data on the possibility of the clinical treatment of Bee Venom in inflammation diseases.

• Molecular & Cellular Toxicology
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• 제5권3호
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• pp.187-192
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• 2009

Toll-like receptors (TLRs) play an important role in host defense by sensing invading microbial pathogens. The stimulation of TLRs by microbial components triggers the activation of the myeloid differential factor 88 (MyD88)- and toll-interleukin-1 receptor domain-containing adapter inducing interferon-$\beta$ (TRIF)-dependent downstream signaling pathways. TLR/MyD88 signaling pathway induces the activation of nuclear factor-kappa B (NF-${\kappa}B$) and the expression of inflammatory cytokine genes, including tumor necrosis factor-alpha, interleukin (IL)-6, IL-12, and IL-$1{\beta}$. On the other hand, TLR/TRIF signaling pathway induces the delayed-activation of NF-${\kappa}B$ and interferon regulatory factor 3 (IRF3), and the expression of type I interferons (IFNs) and IFN-inducible genes. The divalent heavy metal cadmium (Cd) is clearly toxic to most mammalian organ systems, especially the immune system. Yet, the underlying toxic mechanism(s) remain unclear. Cd inhibits the MyD88-dependent pathway by ceasing the activity of inhibitor-${\kappa}B$ kinase. However, it is not known whether Cd inhibits the TRIF-dependent pathway. Presently, Cd inhibited NF-${\kappa}B$ and IRF3 activation induced by lipopolysaccharide (LPS) and polyinosinic-polycytidylic acid. Cd inhibited LPS-induced IRF3 phosphorylation and IFN-inducible genes such as interferon inducible protein-10 and regulated on activation normal T-cell expressed and secreted (RANTES). These results suggest that Cd can modulate TRIF-dependent signaling pathways of TLRs.

• IMMUNE NETWORK
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• 제8권3호
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• pp.90-97
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• 2008

Background: Hypersensitivity pneumonitis (HP) comprises a group of lung diseases resulting from repeated inhalation of various antigens such as Saccharopolyspora rectivirgula (SR). HP is categorized as a Th1 disease. Therefore, it has been suggested that IL-4, Th2 type cytokine, plays a protective role in the development of HP. However, the functional role of IL-4 in HP has not been extensively investigated in vivo. Therefore, we investigated the functional role of IL-4 in HP using IL-4 knockout (KO) mice. Methods: HP was induced by repeated exposure to SR in C57BL/6 (B6) and IL-4 KO (C57BL/6 background) mice. Results: IL-4 KO mice aggravated HP in terms of histological alteration, SR-specific immune responses, and inflammatory cell infiltration in the lungs compared with B6 mice. IL-4 KO mice produced high levels of IFN-${\gamma}$, TGF-${\beta}$ and TNF-${\alpha}$ in the lungs, whereas B6 mice showed the enhanced production of IL-4. Moreover, chemokines such as MIP-1${\alpha}$, MCP-1, and RANTES were highly expressed in IL-4 KO mice. IFN-${\gamma}$-secreting CD4, CD8 T cells, and neutrophils were enhanced in the bronchoalveolar lavage fluid (BALF) of IL-4 KO mice than those of B6 mice. The administration of recombinant(r) IL-4 restored these immunologic parameters in IL-4 KO mice. Conclusion: These results indicate that IL-4 plays a suppressive role in SR-induced HP by attenuating Th1-dominant immune responses.

• 생약학회지
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• 제43권3호
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• pp.231-238
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• 2012

Menthae herba (MH) extracts exhibit anti-inflammatory effects. The purpose of this study was to determine whether the anti-inflammatory effects of MH extracts vary according to the cultivation regions. We performed a comparative analysis of MH extracts by evaluating the production of inflammatory mediators in RAW 264.7 murine macrophage cells and HaCaT human keratinocyte cells. MH extracts obtained from different cultivation regions in Korea and China significantly reduced the production of nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in RAW 264.7 cells stimulated with lipopolysaccharide (LPS). No differences in these inhibitory activities were observed between MH extracts. In HaCaT cells stimulated with TNF-${\alpha}$ and interferon-${\gamma}$ (IFN-${\gamma}$), MH extracts did not inhibit the production of macrophage-derived chemokine (MDC/CCL22), but most extracts reduced the production of the regulated on activation normal T-cell expression and secreted (RANTES/CCL5). We used clustering tree analysis of the MH extracts according to the chromatographic pattern and anti-inflammatory potency of MH extracts. We observed differences in the chromatographic pattern of MH extracts but no difference in anti-inflammatory potency. Our findings suggest that MH extracts from different regions do not show any differences in their pharmacological potency in that MH extracts are used as therapeutic agents to treat inflammatory disorders.

• 대한한방내과학회지
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• 제26권1호
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• pp.199-212
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• 2005

Objective : Airway inflammation is now regarded as a defining feature of asthma. The importance of eosinophits in the airway inflammation of asthma patients is widely recognized, and eosinophils mobilization in the respiratory epithelium is activated by chemoattractants and cytokines. This study was designed to examine the extent of the ability of Moutan Cortex Radicis to inhibit eosinophil chemotaxis of pulmonary epithelium after allergic stimulation. Material and Methods : Water extracts of Moutan Cortex Radicis and pulmonary epithelial cell lines A549(human type II-like epithelial cells) and human eosinophils were used. Cytotoxic effects of Moutan Cortex Radicis were estimated via MTS assay, and the effects of Moutan Cortex Radicis on chemokines from prestimulated A549 cells were estimated by sandwich ELISA and RT-PCR. Chemotaxis assay on prestimulated eosinophils treated with Moutan Cortex Radicis. was conducted Result : In this study we demonstrated that $TNF-{\alpha}$ and IL-4, $IL-1{\beta}$ induced the accumulation of chemokines' mRNA in the pulmonary epithelial cell lines A549 in a dose-dependent manner. Chemokines of eotaxin, ICAM-1, YCAM-1, IL-8, IL-16 were inhibited by Moutan Cortex Radicis in a dose dependent manner, but RANTES showed no inhibition due to Moutan Cortex Radicis. Eosinophil migration was inhibited at high concentrations of Moutan Cortex Radicis. Conculusion : These findings are indicative of supression of chemokines accomplished by Moutan Cortex Radicis treatment, demonstrating the potential therapeutic value of Moutan Cortex Radicis for treating diseases such as asthma.