• Journal of Haehwa Medicine
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• v.17 no.2
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• pp.167-183
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• 2008

KCSYJT medicines controlled $CD4^+/IFN-\gamma$, and $CD4^+/CD25^+/foxp3^+$ revelation that an experiment that motive allergy immune reponse because an in vitro experiment stimulates T cells of a NC/Nga mouse same time by anti-CD40/rmIL-4, and interleukin-$1{\beta}$, IL-6, TNF-$\alpha$, and TGF-$\beta$ mRNA outturn that bear in T and B cells decreased remarkably by KCSYJT medicines. Intracellular staining of splenocytes anti-CD40/rmIL-4 plus rmIL-4 stimulated as described in a, assessed after 24 h, KCSYJT exerts a mainly immunosuppressive effect that acts at least partially through suppression of the transcription factor GATA3 expression in $CD4^+$ T cells. We found that skin lesions, which were clinically and histologically very similar to human AD, mite antigen-induced dermatitis on the face, neck, ears and dorsal skin of inbred NC/Nga mice. Result that Th1 cell and Th2 cell observe to be shifted by cytokine expression with GATA3 regulation by KCSYJT medicines could know that KCSYJT medicines can use usefully in allergy autoimmnune diease.

• Journal of Ginseng Research
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• v.44 no.4
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• pp.593-602
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• 2020

Background: Heat stress orchestrates neurodegenerative disorders and results in the formation of reactive oxygen species that leads to cell death. Although the immunomodulatory effects of ginseng are well studied, the mechanism by which ginseng alleviates heat stress in the brain remains elusive. Methods: Rats were exposed to intermittent heat stress for 6 months, and brain samples were examined to elucidate survival and antiinflammatory effect after Korean Red Ginseng (KRG) treatment. Results: Intermittent long-term heat stress (ILTHS) upregulated the expression of cyclooxygenase 2 and inducible nitric oxide synthase, increasing infiltration of inflammatory cells (hematoxylin and eosin staining) and the level of proinflammatory cytokines [tumor necrosis factor α, interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6], leading to cell death (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) and elevated markers of oxidative stress damage (myeloperoxidase and malondialdehyde), resulting in the downregulation of antiapoptotic markers (Bcl-2 and Bcl-x_L) and expression of estrogen receptor beta and brain-derived neurotrophic factor, key factors in regulating neuronal cell survival. In contrast, KRG mitigated ILTHS-induced release of proinflammatory mediators, upregulated the mRNA level of the antiinflammatory cytokine IL-10, and increased myeloperoxidase and malondialdehyde levels. In addition, KRG significantly decreased the expression of the proapoptotic marker (Bax), did not affect caspase-3 expression, but increased the expression of antiapoptotic markers (Bcl-2 and Bcl-x_L). Furthermore, KRG significantly activated the expression of both estrogen receptor beta and brain-derived neurotrophic factor. Conclusion: ILTHS induced oxidative stress responses and inflammatory molecules, which can lead to impaired neurogenesis and ultimately neuronal death, whereas, KRG, being the antioxidant, inhibited neuronal damage and increased cell viability.

• Journal of Microbiology and Biotechnology
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• v.23 no.3
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• pp.414-421
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• 2013

Lactic acid bacteria (LAB) in fermented foods have attracted considerable attention recently as treatment options for immune diseases, the incidence of which has been increasing worldwide. The ability of 500 strains of LAB, isolated from kimchi, to induce TNF-${\alpha}$ production in peritoneal macrophages was investigated. Lactobacillus plantarum HY7712 most strongly induced TNF-${\alpha}$ production as well as NF-${\kappa}B$ activation. However, HY7712 inhibited NF-${\kappa}B$ activation in LPS-stimulated peritoneal macrophages. When HY7712 was orally treated in cyclophosphamide (CP)-immunosuppressed mice for 5 or 15 days, it reversed the body and spleen weights, blood RBC and WBC levels, and splenocyte and bone marrow cells that were reduced by CP. Orally administered HY7712 increased concanavalin A-induced T cell proliferation to 84.5% of the normal group on day 15, although treatment with CP alone markedly reduced it to 53.7% of the normal group. Furthermore, orally administered HY7712 significantly induced the expressions of IL-2 and IFN-${\gamma}$ in ConA-induced splenic cytotoxic T cells of CP-treated mice. Orally administered HY7712 restored the CP-impaired phagocytosis of macrophages in mice. Orally administered HY7712 also restored the cytotoxicity of NK and cytotoxic T cells derived from spleen and bone marrow against YAC-1 in CP-immunosuppressed mice. Based on these findings, orally administered HY7712 may accelerate the recovery of cyclophosphamide-caused immunosuppression, without evident side effects, by immunopotentiating NK and Tc cells, and may provide a mechanistic basis for using HY7712 as an alternative means in lessening chemotherapyinduced immunosuppression in cancer patients.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.10
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• pp.1329-1335
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• 2006

LP-BM5 murine leukemia retrovirus induces the excessive oxidative stress and immune dysfunction leading to B cell leukemia and murine AIDS with cytokine dysfunction. In the present study, the immune restoratory effect of antioxidant hormone dedydroepiandrosterone sulfate (DHEAS) was investigated in the primary splenocytes from LP-BM5 retrovirus-infected C57BL/6 mice. DHEAS significantly increased T and B cell response to mitogen and normalized the unbalanced production of Th1/Th2 type cytokines. In particular, both protein and mRNA expression of IL-4, IL-6, and $TNF-\alpha$ were down-regulated by DHEAS treatment whereas IL-2 and $IFN-\gamma$ level were increased. This result suggests that DHEAS directly or indirectly regulates the gene expression of Th1/Th2 type cytokines in transcription level. In addition, DHEAS treatment decreased the hepatic lipid peroxidation and preserved vitamin E level in liver cells. These results suggested that DHEAS could effectively prevent immune dysfunction by regulating cytokine secretion and preventing the oxidative stress in murine AIDS.

• Biomedical Science Letters
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• v.24 no.3
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• pp.213-220
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• 2018

Triglyceride (TG) is known to be associated with inflammatory disease including atherosclerosis. In a variety of atherosclerosis models, T lymphocytes are localized in the earliest lesions of atherosclerosis. T cell associated cytokines such as $TNF-{\alpha}$ and $IFN-{\gamma}$ have pre-dominant inflammatory effects in chronic vascular diseases. In our previous study, we found that the expression of $TNF-{\alpha}$ and its receptor, $TNF-{\alpha}R$ was increased when Jurkat T lymphocyte cell lines were exposed to TGs. Therefore, experiments were conducted to determine which cell signaling pathway are involved in the increase of $TNF-{\alpha}$ and $TNF-{\alpha}R$ expression by TGs. To identify signal transduction pathways involved in TG-induced upregulation of $TNF-{\alpha}$, we treated TG-exposed Jurkat T cells with specific inhibitors for MEK1, PI3K, $NF-{\kappa}B$ and PKC. We found that inhibition of the MEK1 pathway blocked TG-induced upregulation of $TNF-{\alpha}$. However, the expression level of $TNF-{\alpha}R$ did not change with any signal transduction inhibitor. Based on this observation, we suggest that increase of exogenous TG induces increase of $TNF-{\alpha}$ expression through MEK1 pathway in Jurkat T cells. In addition, it was confirmed that the increase of $TNF-{\alpha}$ and $TNF-{\alpha}R$ expression by TGs occurs via different pathways.

• Journal of Ginseng Research
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• v.36 no.4
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• pp.383-390
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• 2012

Ginseng has been used as an herbal medicine, widely used in Asian countries, for long time. Recently, beneficial effects for immune functions of Korean red ginseng (KRG) have been reported in adults. This study was performed to investigate the effects of ginseng on immune functions in children after cessation of chemotherapy or stem cell transplantation for advanced cancer. Thirty patients, who were diagnosed and treated for leukemia and solid cancer at the department of pediatrics and adolescence of the Yeungnam University Hospital from June 2004 to June 2009, were enrolled for the study. The study group consisted of 19 patients who received KRG extract (60 mg/kg/d) for 1 yr and 11 patients who did not receive KRG extract were the control group. Blood samples were collected every 6 mo. Immune assays included circulating lymphocyte subpopulation, serum cytokines (IL-2, IL-10, IL-12, TNF-alpha, and IFN-gamma), and total concentrations of serum IgG, IgA, and IgM subclasses. Age at diagnosis ranged from 2 mo to 15 yr (median 5 yr). Nine patients received stem cell transplantation. The cytokines of the KRG treated group were decreasing more rapidly than that of the control group. Lymphocyte subpopulations (T cell, B cell, NK cell, T4, T8, and T4/T8 ratio) and serum immunoglobulin subclasses (IgG, IgA, and IgM) did not show significant differences between the study and the control groups. This study suggests that KRG extract might have a stabilizing effect on the inflammatory cytokines in children with cancer after chemotherapy.

• YAKHAK HOEJI
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• v.51 no.1
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• pp.35-43
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• 2007

To investigate the immunomodulatory roles of cyclic AMP (CAMP) on macrophage- and T lymphocyte-mediated immune responses, CAMP elevating agents were employed and carefully re-examined under the activation conditions of the cells. Various inhibitors tested dose-dependently blocked tumor necrosis factor (TNF)-${\alpha}$ production with IC$_{50}$ values ranged from 0.04 to 300 ${\mu}$M. Of the inhibitors, cAMP-elevating agents showed lower cytotoxicity assessed by lactate dehydrogenase (LDH) release, suggesting less toxic and more selective. In particular co-treatment of dbcAMP with a protein kinase C inhibitor staurosporine displayed the synergistic inhibition of TNF-${\alpha}$ production. The modulatory effect of dbcAMP on TNF-${\alpha}$ and nitric oxide (NO) was significantly affected by treatment time of dbcAMP. Thus, post-treatment of dbcAMP (three hours before LPS) abrogated dbcAMP's inhibitory activity and rather enhanced TNF-${\alpha}$ level up to 60%. In contrast, additional NO production was shown at the co-treatment of dbcAMP with LPS. Unlike simultaneous treatment of phorbol 12-myristate 13-acetate (PMA) and interferon (IFN)-${\gamma}$co-treatment, the combination of dbcAMP with other NO-inducing stimuli did not show drastic overproduction of NO. cAMP elevating agents also diminished splenocyte proliferation stimulated by concanavalin (Con) A, phytohemaglutinin A (PHA) and lipopolysaccharide (LPS). In addition, dbcAMP but not rolipram strongly suppressed CD8$^+$ T cells (CTLL-2). Finally, cAMP elevating agents were differentially involved in regulating CD98-mediated cell-cell adhesion. Thus, dbcAMP and rolipram significantly enhanced the cell-cell adhesion, whereas forskolin blocked. Therefore, our results suggest that CAMP elevating agents participate in various immune responses mediated by macrophages and T cells with a different fashion depending on cellular environments and activation signals.

• Archives of Pharmacal Research
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• v.27 no.2
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• pp.217-224
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• 2004

Previously, we reported that water-extracted Acanthopanax senticasus exhibited anti-meta-static activity by stimulating the immune system. In this study, we fractionated glycoproteins (EN-SP) from the soluble protein layer (GF-AS) of A. senticasus and determined their basic chemical properties. We also investigated the anti-tumor and immunostimulating activities of the fractionated glycoprotein, EN-SP. We found that intravenous (i.v.) administration of GF-AS dramatically inhibited metastasis of colon26-M3.1 carcinoma cells to the lung in a dose-dependent manner. In vitro analysis showed GF-AS to enhance the proliferation of splenocytes. GF-AS also stimulated peritoneal macrophage, which was followed by the production of various cytokines such as IL-1$\beta$, TNF-$\alpha$, IL-12 and IFN-${\gamma}$. Furthermore, the production of these cytokines was partially blocked when peritoneal macrophage was cultured with the polyclonal antibodies against GF-AS. The depletion of NK cells by rabbit anti-asialo GM1 serum partly abolished the inhibitory effect of GF-AS on lung metastasis of colon26-M3.1 cells. Using gel filtration, EN-SP, an active glycoprotein fraction, is isolated from GF-AS. While both GF-AS and EN-SP stimulated the proliferatation of splenocytes of normal mice, EN-SP showed higher anti-metastatic activity and more potently stimulated the proliferation of splenocytes compared to GF-AS. These results suggest the use of EN-SP, the fractionated glycoprotein from A. senticasus, can be used as a therapeutical reagent to prevent or inhibit tumor metastasis.

• Journal of Haehwa Medicine
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• v.16 no.2
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• pp.131-145
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• 2007

To evaluate the effects of GP on contact dermatitis, we examined the composition of immune cells from drain lymph node in DNCB-induced contact dermatitis murine model NC/Nga mice. And the amount of pathologic cytokines of spleen and antioxidant activity were investigated. The results were summarized as followers; 1. GP did not show cytotoxic effect on mLFC in vitro. 2. GP did not have hepatotoxicity in vivo in the level of ALT, AST. 3. GP decreased the production of DPPH and in a dose-dependent. 4. GP significantly decreased total cell number of DLN in DNCB-induced NC/Nga mice compared to the untreated control group. 5. GP significantly decreased the number of CD3+, CD19+, CD4+, CD8+, CD3+/CD69+ and CD4+/CD45+ in DLN of DNCB-induced NC/Nga mice compared to the untreated control group. 6. GP significantly reduced the level of IL-4 and IFN-$\gamma$ in splenocytes of DNCB-induced NC/Nga mice compared to the untreated control group. Taken together above results, GP have therapeutic effects on contact dermatitis by regulating T cell activation. This study warranted further investigations of molecular mechanisms of GP on contact dermatitis.

• Journal of Environmental Health Sciences
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• v.31 no.4 s.85
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• pp.287-293
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• 2005

Pollen has been used for Prevention or treatment of certain diseases such as diabetes, arthritis, or cancer in traditional medicine. In addition, pollen is under investigation as a host cell for a gene expression. This study was undertaken to evaluate the immunologic safety of pollen intake. BALB/c mice were administered with 500, 50,5, or 0.5 mg/kg bw of lily pollen for five times a week for four weeks through gastric intubation. Comparing the control mice administered with distilled water, no significant changes were observed in body weight gain, weight of liver, spleen, lung, and his-topathological findings of liver and kidney of the mice groups administered with the pollen. Plasma level of IgG1, IgG2a, and IgE was not different among the groups. When splenic B lymphocytes were stimulated in vitro with lipopolysaccharides for 7 days, level of IgGl and IgGwa produced in the culture supernatants was not significantly different among the groups. Furthermore, no significant alteration was observed in IL-4 and $IFN{\gamma}$ producing ability with splenic T lymphocytes stimulated in vitro with phytohemagglutinins for 48 hours between the pollen-administered and the control mice. Overall, this study suggests that the lily pollen intake is Inducing no significant modulation of humoral and cell-mediated immunity in mice.