• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.264.1-264.1
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• 2003

In order to search for the anti-HIV agents from natural products, Eighty MeOH extracts of medicinal plants were applied to a syncytia formation inhibition assay which is based on the interaction between the HIV-1 envelope glycoprotein gp120/gp41 and the cellular membrane protein CD4 of T lymphocytes. Among them, Ailanthus altissima showed a potent virus-cell fusion inhibitory activity. (omitted)

• 동의생리병리학회지
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• 제23권1호
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• pp.41-49
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• 2009

Soeumin-Googwihyangso-san(SGGHSS) has been used for the prevention or treatment of Soeumin-allergic rhinitis. This study was performed to demonstrate anti-allergic and anti-inflamatory effects of SGGHSS methanol extract in HMC cell lines and activated mouse B cells and CD4+ T cells. SGGHSS inhibited the production of TNF-$\alpha$ in PMA plus A23187 activated HMC-1 cells but not that of IL-6, as measured by ELISA. SGGHSS inhibited the expression of CD23 and surface IgE in B cells as determined by flowcytometry. It also inhibited secretion of IFN-$\gamma$ and IgG1, the Th1 related IgG type, but increased that of IL-4 in anti-CD40 and IL-4 treated B cells as measured by ELISA. As for Th cell differentiation, SGGHSS did not much affect IL-4 or IFN-$\gamma$. Taken together, our data showed that SGGHSS exerted an anti-inflammtory effect by inhibiting TNF-$\alpha$ in mast cells and has anti-allergic activity not via inhibition of CD4+ T cell, but via inhibition of B cells. These results suggest some evidence that SGGHSS can be applied to allergic disease.

• 약학회지
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• 제42권3호
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• pp.296-301
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• 1998

To investigate the effects of ginsenosides from Panax ginseng on mitogenic responses in macrophages and splenocytes from murine, we examined the effects of representative protopanaxadiol and protopanaxatriol ginsenosides ($Rb_1,\;Rb_2,\;Re\;and\;Rg_1$) on tumor necrosis factor-${\alpha}$ (TNF-(${\alpha}$) production in murine macrophage cell line (RAW264.7 cells) stimulated by lipopolysaccharide (LPS) and T cell proliferation in splenocytes stimulated by concanavalin A (Con A). Among the ginsenosides tested, protopanaxadiol ginsenosides ($Rb_1\;and\;Rb_2$) significantly inhibited TNF-${\alpha}$ production in a dose-dependent manner. However, protoppanaxatriol ginsenosides (Re and $Rg_1$) showed little inhibitory activity. The molar concentrations of $Rb_1\;and\;Rb_2$ producing 50% inhibition ($IC_{50}$) of TNF-${\alpha}$ production were $55.8{\mu}g/ml\;(48.0{\mu}M)\;and\;31.8{\mu}g/ml (27.9{\mu}M)$, respectively. As a positive control, prednisolone also exhibited inhibitory activity with an $IC_{50}$ value of $21.7{\mu}M$. In T cell proliferation, $Rg_1$, was not effective but $Rb_1$ and Re or $Rb_2$ significantly increased or inhibited at high concentration, 75 and $100{\mu}g/ml$. In contrast, prednisolone showed potent inhibitory activity with an $IC_{50}$ value of 6.1nM. These results suggest that ginsenosides may take part in the mitogen-induced signaling pathway for TNF-${\alpha}$ production and T cell proliferation from macrophages and splenocytes.

• 한국축산식품학회지
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• 제25권4호
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• pp.494-499
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• 2005

본 연구에서는 유아의 분변에서 분리한 항산화 효과를 갖는 유산균인 Lactobacillus gasseri KACC 91155의 Jurkat T cell line에서의 지질 과산화 억제 효과, 세포 보호 효과 및 DNA 손상 억제 효과를 측정하였다. 그 결과 1. gasseri 91155는 세포 산화에 의해 생성된 지질 과산화물인 MDA의 생성을 방지하였으며, 또한 뚜렷하게 세포 생존성을 증가시켰다. 그리고 산화적 손상으로부터 DNA 손상을 줄여주는 효과를 나타내었다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권8호
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• pp.3659-3665
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• 2014

To assess inhibition mechanisms of a Phellinus igniarius (PI) extract on cancer, C57BL/6 mice were orally treated with PI extractive after or before implanting H22 (hepatocellular carcinoma ) or B16 (melanoma) cells. Mice were orally gavaged with different doses of PI for 36 days 24h after introduction of H22 or B16 cells. Mice in another group were orally treated as above daily for 42 days and implanted with H22 cells on day 7. Then the T lymphocyte, antibody, cytokine, LAK, NK cell activity in spleen, tumor cell apoptosis status and tumor inhibition in related organs, as well as the expression of iNOS and PCNA in tumor tissue were examined. The PI extract could improve animal immunity as well as inhibit cancer cell growth and metastasis with a dose-response relationship. Notably, PI's regulation with the two kinds of tumor appeared to occur in different ways, since the antibody profile and tumor metastasis demonstrated variation between animals implanted with hepatocellular carcinoma and melanoma cells.

• IMMUNE NETWORK
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• 제14권6호
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• pp.265-276
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• 2014

The interactions between B7 molecules and CD28-family receptors are crucial in the regulation of adaptive cellular immunity. In cancer, the aberrant expression of co-inhibitory B7 molecules has been attributed to reduced anti-tumor immunity and cancer immune evasion, prompting the development of cancer therapeutics that can restore T cell function. Murine tumor models have provided significant support for the targeting of multiple immune checkpoints involving CTLA-4, PD-1, ICOS, B7-H3 and B7-H4 during tumor growth, and clinical studies investigating the therapeutic effects of CTLA-4 and PD-1 blockade have shown exceptionally promising results in patients with advanced melanoma and other cancers. The expression pattern of co-inhibitory B7 ligands in the tumor microenvironment has also been largely correlated with poor patient prognosis, and recent evidence suggests that the presence of several B7 molecules may predict the responsiveness of immunotherapies that rely on pre-existing tumor-associated immune responses. While monotherapies blocking T cell co-inhibition have beneficial effects in reducing tumor burden, combinatorial immunotherapy targeting multiple immune checkpoints involved in various stages of the anti-tumor response has led to the most substantial impact on tumor reduction. In this review, we will examine the contributions of B7- and CD28-family members in the context of cancer development, and discuss the implications of current human findings in cancer immunotherapy.

• Archives of Pharmacal Research
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• 제29권1호
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• pp.59-63
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• 2006

Secalonic acid D(SAD) was isolated as the major secondary metabolite of the marine lichen-derived fungus Gliocladium sp. T31. Its structure was established on the basic of physicochemical and spectroscopic data. This is the first report on the isolation of SAD from this fungus, as well as its inhibitory effect on K562 cell cycle and its cytotoxicity against several tumor cell lines in vitro.

• Biomolecules & Therapeutics
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• 제21권3호
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• pp.196-203
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• 2013

Recent accumulating studies have reported that hypoxic preconditioning during ex vivo expansion enhanced the self-renewal or differentiation of various stem cells and provide an important strategy for the adequate modulation of oxygen in culture conditions, which might increase the functional bioactivity of these cells for cardiac regeneration. In this study, we proposed a novel priming protocol to increase the functional bioactivity of cardiac progenitor cells (CPCs) for the treatment of cardiac regeneration. Firstly, patient-derived c-$kit^+$ CPCs isolated from the atrium of human hearts by enzymatic digestion and secondly, pivotal target molecules identified their differentiation into specific cell lineages. We observed that hCPCs, in response to hypoxia, strongly activated ERK phosphorylation in ex vivo culture conditioning. Interestingly, pre-treatment with an ERK inhibitor, U0126, significantly enhanced cellular proliferation and tubular formation capacities of CPCs. Furthermore, we observed that hCPCs efficiently maintained the expression of the c-kit, a typical stem cell marker of CPCs, under both hypoxic conditioning and ERK inhibition. We also show that hCPCs, after preconditioning of both hypoxic and ERK inhibition, are capable of differentiating into smooth muscle cells (SMCs) and cardiomyocytes (CMs), but not endothelial cells (ECs), as demonstrated by the strong expression of ${\alpha}$-SMA, Nkx2.5, and cTnT, respectively. From our results, we conclude that the functional bioactivity of patient-derived hCPCs and their ability to differentiate into SMCs and CMs can be efficiently increased under specifically defined culture conditions such as short-term hypoxic preconditioning and ERK inhibition.

• Molecules and Cells
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• 제28권6호
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• pp.553-558
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• 2009

In the periphery, a galectin-1 receptor, CD7, plays crucial roles in galectin-1-mediated apoptosis of activated T-cells as well as progression of T-lymphoma. Previously, we demonstrated that $NF-{\kappa}B$ downregulated CD7 gene expression through the p38 MAPK pathway in developing immature thymocytes. However, its regulatory pathway is not well understood in functional mature T-cells. Here, we show that CD7 expression was downregulated by Twist2 in Jurkat cells, a human acute T-cell lymphoma cell line, and in EL4 cells, a mature murine T-cell lymphoma cell line. Furthermore, ectopic expression of Twist2 in Jurkat cells reduced galectin-1-induced apoptosis. While full-length Twist2 decreased CD7 promoter activity, a C-terminal deletion form of Twist2 reversed its inhibition, suggesting an important role of the C-terminus in CD7 regulation. In addition, CD7 expression was enhanced by histone deacetylase inhibitors such as trichostatin A and sodium butyrate, which indicates that Twist2 might be one of candidate factors involved in histone deacetylation. Based on these results, we conclude that upregulation of Twist2 increases the resistance to galectin-1-mediated-apoptosis, which may have significant implications for the progression of some T-cells into tumors such as Sezary cells.

• 대한의용생체공학회:의공학회지
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• 제39권4호
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• pp.168-174
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• 2018

Adipocytes affect obesity through the regulation of lipid metabolism. Physical loading is an important regulator of fat tissue. There are ongoing in vitro studies inducing mechanotransduction on 3T3-L1 preadipocytes with mechanical stimulus in order to treat obesity by inhibiting adipogenesis and provoking cell death. In this study, our goal was to suggest a new therapy for obesity by investigating whether fluid shear stress (FSS) changes transcription factors on 3T3-L1 related with adipogenesis and cell death. FSS loading was applied to 3T3-L1 preadipocytes at 1Pa and 1Hz. After loading, bright field images were taken and an immunofluorescence assay was conducted to observe actin stress fiber formation. Western blot analysis was conducted to identify the activation of the ERK pathway as well as the adipogenic factors, which including C/EBPs and $PPAR{\gamma}$. The expression of osteopontin, a protein related to inflammation in adipose tissue, and cell death related factors, Bax, Bcl-2, and Beclin, were also measured. Results showed that FSS stimulated the formation of actin stress fibers in 3T3-L1 and also that the activation of C/EBPs decreased significantly when compared with the control group. $PPAR{\gamma}$ activation in the 2 hour FSS group was lower than the 1 hour FSS group, which implied that the results were time dependent. Additionally, there were no differences in the expression of cell death factors after FSS loading. In summary, similar to other fibroblasts, the formation of actin stress fibers induced by mechanotransduction may affect the differentiation of 3T3-L1, leading to inhibition of adipogenesis and inflammation.