• The Journal of Pediatrics of Korean Medicine
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• v.24 no.2
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• pp.126-136
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• 2010

Objectives The purpose of this study was to investigate the antiallergic and antioxidative effects of Chaenomeles Sinensis (CS). Methods CS pretreatments inhibited anti-DNP IgE in RBL-2H3 mast cells for an hour. we measured cell viability, $\beta$-hexosaminidase release, IL-4, TNF-$\alpha$ secretion, and IL-4, TNF-$\alpha$ mRNA expression CS pretreatments inhibited DNP-HSA($10\;{\mu}g/ml$) for ten minutes, we measured Dicholrodihydrofluorescein(DCF) and DPPH radical-scavenging activity in 0.5 mM 1,1-diphenyl-2-picrydrazyl(DPPH) radical solution, 0.1ml, 99% ethanol 0.8ml, and CS 0.1 ml mixed solution. Results 0, 1, 2, 3, 4, 5 mg/ml CS treatments were not affect on cell viability and inhibited b-hexosaminidase release, IL-4, TNF-$\alpha$ secretion, CS treatments also decreased IL-4, TNF-$\alpha$ mRNA expression in RBL-2H3 cells. CS treatments inhibited reactive oxygen species(ROS) and DPPH radical-scavenging activity. Conclusions These results suggest that CS may be useful for the prevention or treatment of allergic disease.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.6
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• pp.319-325
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• 2002

The induction of interleukin-6 (IL-6) using combined proinflammatory agents $(LPS/IFN-{\gamma}\;or\;TNF-{\alpha}/IFN-{\gamma})$ was studied in relation to p38 mitogen-activated protein kinase (MAPK) and $NF-{\kappa}B$ transcriptional factor in primary neonatal cardiomyocytes. When added to cultures of cardiomyocytes, the combined agents $(LPS/IFN-[\gamma}\;or\;TNF-{\alpha}/IFN-{\gamma})$ had stimulatory effect on the production of IL-6 and the elevation was significantly reduced by SB203580, a specific p38 MAPK inhibitor. SB203580 inhibited protein production and gene expression of IL-6 in a concentration-dependent manner. In this study, $IFN-{\gamma}$ enhancement of $TNF-{\alpha}-induced\;NF-{\kappa}B$ binding affinity as well as p38 MAP kinase activation was observed. However, a specific inhibitor of p38 MAPK, SB203580, had no effect on $TNF-{\alpha}/IFN-{\gamma}\;or\;LPS/IFN-{\gamma}-induced\;NF-{\kappa}B$ activation. This study strongly suggests that these pathways about $TNF-{\alpha}/IFN-{\gamma}$ or $LPS/IFN-{\gamma}-activated$ IL-6 release can be primarily dissociated in primary neonatal cardiomyocytes.

• Archives of Pharmacal Research
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• v.26 no.3
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• pp.244-251
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• 2003

Plant nutrients are believed to provide protection against various diseases including inflammation. Since interactions of the cell adhesion molecules are known to play important roles in mediating inflammation, inhibiting adhesion protein upregulation is a possible therapeutic target. In this study, the interacellular adhesion molecule-1 (ICAM-1) was induced in human umbilical endothelial cells (HUVECs) after stimulation with $TNF-{\alpha}$. In addition, alginate, ascorbic acid and allicin were demonstrated to inhibit the $TNF-{\alpha}$ induced expression of ICAM-1 on the HUVECs in a dose-dependent manner. These compounds also inhibited the production of NO and $H_2O_2$ induced by $TNF-{\alpha}$, which suggests that the inhibition of ICAM-1 expression by the three compounds may be due to the modulated production of the reactive oxygen/nitrogen components. Overall, these results indicate that these dietary components have a therapeutic potential in the treatment of various inflammatory disorders associated with an increase in endothelial leukocyte adhesion molecules.

• Journal of Chest Surgery
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• v.33 no.1
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• pp.1-6
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• 2000

Background: TNF-$\alpha$ plays a major role in producing left ventricular dysfunction cardio-myopathy pulmonary edema and inhibits the compensatory mechanism of congestive heart failure. IL-6 is an acute reactant of immune reaction and also known to control immune reaction but its function in the myocyte was not clearly investigated. Author's performed this experiment to investigate the contents of TNF-$\alpha$ and IL-6 on the assumption that TNF-$\alpha$ and IL-6 may reside in nonfailing heart that has gone cardiac surgery and play some role in cardiac function. Material and Method : Right auricular tissues were sampled from 12 patients who had undergone total corrective surgery for both congenital and acquired heart diseases from January 1998 to June 1998 in Kosin Universcfy Gospel hospital. The quantitive analysis of TNF-$\alpha$ and IL-6 were assessed by ELISA method in right auricular tissue. Hemodynamic values about the pressure of ventricle atrium aorta pulmonary artery and cardiac index pulmonary and systemic vascular resistance and cardiac output were measured by echocardiography and cardiac catheterization and biochemical analyses of LDH & AST were done before operation. statistical analysis was by Paired Student t-test. Patients were divided into children(under 15 years olds) and adults groups and the data was compared beween two groups. Conclusion: Mild pulmonary hypertension and increased pulmonary vascular resistance were existed in both group. The contents of tissue TNF-$\alpha$ IL-6 in each group were independent of each data.

• Journal of Microbiology
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• v.39 no.3
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• pp.186-194
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• 2001

Scrub typhus, caused by Orientia tsutsugamushi infection, is clinically and histopathologically characterized by local as well as systemic inflammatory reactions, indicating that orientiae induce mechanisms that amplify the inflammatory response. To reveal underlying mechanisms of chemoattraction and activation of responding leukocytes, expression of chemokine and tumor necrosis factor alpha (TNF-$\alpha$) genes in murine peritoneal macrophages after infection with the obligate intracellular bacterium Ο.tsutsugamushi was investigated. The genes that were unregulated included macrophage inflammatory proteins l$\alpha$/$\beta$(MIP-l$\alpha$/$\beta$), MIP-2, monocyte chemoattractant protein 1(MCP-1), RANTES (regulated upon activation, normal T-cell expressed and secreted), gamma-interferon-inducible protein 10(IP-10) and TNF-$\alpha$. Peak expression of these chemokines and TNF-$\alpha$ was observed between 1 and 3 h after infection. These responses returned to or approached baseline preinfection levels 6 h after challenge. Semiquantitative reverse transcription (RT)-PCR analysis revealed dramatic Increases during infection in the steady-state levels of mRNA ceding for the inhibitory subunit of NF-kB (IkB$\alpha$), whose transcription is enhanced by binding of NF-kB within the IkB$\alpha$promoter region. Thus, Ο. tsutsugamushi appears to be a stung inducer of chemokines and TNF-$\alpha$ which may significantly contribute to inflammation and tissue damage observed in scrub typhus by attracting and activating phagocytic leukocytes.

• Tuberculosis and Respiratory Diseases
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• v.69 no.5
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• pp.348-353
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• 2010

Background: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-${\alpha}$-induced MUC5AC mucin production and gene expression from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-${\alpha}$ for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Results: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-${\alpha}$; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-${\alpha}$. Conclusion: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-${\alpha}$, by directly acting on airway epithelial cells.

• IMMUNE NETWORK
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• v.14 no.2
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• pp.67-72
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• 2014

The herpes virus entry mediator (HVEM) is a member of the tumor necrosis factor receptor superfamily (TNFRSF), and therefore it is also known as TNFRSF14 or CD270 (1,2). In recent years, we have focused on understanding HVEM function in the mucosa of the intestine, particularly on the role of HVEM in colitis pathogenesis, host defense and regulation of the microbiota (2-4). HVEM is an unusual TNF receptor because of its high expression levels in the gut epithelium, its capacity to bind ligands that are not members of the TNF super family, including immunoglobulin (Ig) superfamily members BTLA and CD160, and its bi-directional functionality, acting as a signaling receptor or as a ligand for the receptor BTLA. Clinically, Hvem recently was reported as an inflammatory bowel disease (IBD) risk gene as a result of genome wide association studies (5,6). This suggests HVEM could have a regulatory role influencing the regulation of epithelial barrier, host defense and the microbiota. Consistent with this, using mouse models, we have revealed how HVEM is involved in colitis pathogenesis, mucosal host defense and epithelial immunity (3,7). Although further studies are needed, our results provide the fundamental basis for understanding why Hvem is an IBD risk gene, and they confirm that HVEM is a mucosal gatekeeper with multiple regulatory functions in the mucosa.

• Biomedical Science Letters
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• v.20 no.1
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• pp.32-38
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• 2014

Potassium cyanate (KOCN) that is known as an inducer of the protein carbamylation is an inorganic compound and is the conjugate based of cyanic acid (HOCN). Based on these studies, we confirmed that KOCN induces the apoptosis of the human colorectal cancer cell line, HCT 116 cells, by various mitochondrial pathways. To investigate other mechanisms of KOCN-mediated apoptosis, in the present study, we examined KOCN-induced cytokines production in HCT 116 cells and identified the intracellular signaling pathway in these processes. We first demonstrated that KOCN considerably increased the cell apoptosis via intracellular $Ca^{2+}$ signaling, mitochondrial dysfunction and ROS production. And then we examined TNF-${\alpha}$ and IL-$1{\beta}$ levels mediated by KOCN in HCT 116 cells. Although IL-$1{\beta}$ was not involved in KOCN-mediated HCT 116 cell apoptosis, the release of TNF-${\alpha}$ was mediated by KOCN in HCT 116 cells via NF-${\kappa}B$ activation. Apoptosis was also enhanced by incubation with supernatants from HCT 116 cells after KOCN treatment and this effect was partially reduced by BAY 11-7085 pre-treated supernatant. Taken together, our results indicate that KOCN-induced apoptosis in HCT 116 cells is dependent on the releases of TNF-${\alpha}$ and the increased factors and that the mechanism involves the activation of NF-${\kappa}B$.

• Natural Product Sciences
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• v.18 no.4
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• pp.254-260
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• 2012

Adipose inflammation is linked to the development of insulin resistance and type 2 diabetes. Hesperidin (HES) is a flavonoid with antioxidant, anti-inflammatory and anti-diabetic properties. However, whether HES improves inflammation-mediated insulin resistance in adipose tissues remains unclear. The purpose of this study was to investigate whether HES attenuates inflammation-mediated insulin resistance in adipose tissue. Herein, RAW 264.7 cells and differentiated 3T3-L1 adipocytes were pretreated with various concentrations of HES in complete media for 1 h and then cultured in the presence or absence of LPS or TNF-${\alpha}$. Our results demonstrated that HES remarkably inhibited LPS-induced production of IL-6, TNF-${\alpha}$, and NO by RAW 264.7 cells in a dose-dependent manner. Also, HES inhibited TNF-${\alpha}$-induced production of IL-6 and $PGE_2$ in differentiated 3T3-L1 cells, while upregulated TNF-${\alpha}$-suppressed expression of adiponectin and PPAR-${\gamma}$ mRNA. These findings suggest that HES may ameliorate inflammation-mediated insulin resistance in adipose tissue.

• Natural Product Sciences
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• v.19 no.4
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• pp.316-323
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• 2013

Adipose tissue-derived chronic inflammation contributes to development of insulin resistance in obesity, leading to type 2 diabetes and cardiovascular disease. Baicalin, a flavonoid, has antioxidant, anti-inflammatory, antihyperglycemic, anti-adipogenic, and antiobesity effects. However, whether baicalin attenuates adipose tissue-derived development of insulin resistance remains still unclear. This study was to investigate effect of baicalin on the inflammatory changes involved in the development of insulin resistance in adipose tissue. RAW 264.7 cells and differentiated 3T3-L1 adipocytes were pretreated with various concentrations of baicalin in complete media for 1 h and then cultured in the presence or absence of LPS or TNF-${\alpha}$. Our results demonstrated that baicalin remarkably inhibited LPS-induced production of TNF-${\alpha}$, IL-6, and NO by RAW 264.7 cells in a dose-dependent manner. Baicalin also inhibited TNF-${\alpha}$-induced production of IL-6 and $PGE_2$ in differentiated 3T3-L1 cells in a dose-dependent manner, while upregulated TNF-${\alpha}$-suppressed expression of adiponectin and PPAR-${\gamma}$ mRNA and IRS-1 protein. These findings suggest that baicalin may prevent the adipose tissue-derived development of insulin resistance in obesity.