• Microbiology and Biotechnology Letters
• /
• v.33 no.3
• /
• pp.231-235
• /
• 2005

Histamine-releasing factors (HRFs) are soluble mediators that can release histamine and other mediators from basophils and mast cells and their activity can vary, depending on the type of IgE. The activity of HRFs is affected by the presence of IgE, although HRF is thought to bind to a specific receptor other than IgE. Until now, HRF signaling pathway including its receptor remains unclear in spite of numerous studies. Since there had been many reports about reactive oxygen species (ROS) as a signaling molecule rather than as a by-product of metabolism, we investigated the possibility of ROS as an intracellular messenger involved in HRF-mediated histamine degranulation. In RBL-2H3 cells, ROS was generated by HRF using $H_2O_2$-sensitive fluorescence of fluorescent 2', 7'-dichlorofluorescein ($H_2DCFDA$). These effects were blocked by anti-oxidant N-acetylcysteine (NAC). These results suggest that ROS generation could play a role as an intracellular messenger in histamine release by HRF.

• Applied Microscopy
• /
• v.41 no.1
• /
• pp.21-29
• /
• 2011

Balneotherapy has been widely used for the treatment of skin diseases in the world. The purpose of this study was to determine the bath effect of the alkaline reduced spring water with the properties of high pH and low oxidation reduction potential (ORP) on the skin injury induced by ultra violet (UV) irradiation. For this purpose, hairless mice were irradiated with UV-B to cause skin injury, and individually taken a bath in spring water (experimental group) and tap water (control group) once a day for 40 min during 21 days. We observed histological changes of the back skin through macro- and microscopic methods compared to the control group. We found that skin injury of the experimental group was more quickly recovered than that of the control group. Under the light microscope, the experimental group showed that epidermal thickening (p<0.01) and the mast cell activation (p<0.001) were lower compared with the control group, in addition infiltration of inflammatory cells and degranulation of mast cells were less observed. These results suggest that regular bath in the spring water with the properties of high pH and low ORP has a positive effect on the skin injury induced by UV irradiation.

• Biomolecules & Therapeutics
• /
• v.20 no.1
• /
• pp.43-49
• /
• 2012

Stimulation of mast cells through the high affinity IgE receptor (Fc${\varepsilon}$RI) induces degranulation, lipid mediator release, and cytokine secretion leading to allergic reactions. Although various signaling pathways have been characterized to be involved in the Fc${\varepsilon}$RI-mediated responses, little is known about the precious mechanism for the expression of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in mast cells. Here, we report that rapamycin, a specific inhibitor of mammalian target of rapamycin (mTOR), reduces the expression of TNF-${\alpha}$ in rat basophilic leukemia (RBL-2H3) cells. IgE or specific antigen stimulation of RBL-2H3 cells increases the expression of TNF-${\alpha}$ and activates various signaling molecules including S6K1, Akt and p38 MAPK. Rapamycin specifically inhibits antigeninduced TNF-${\alpha}$ mRNA level, while other kinase inhibitors have no effect on TNF-${\alpha}$ mRNA level. These data indicate that mTOR signaling pathway is the main regulation mechanism for antigen-induced TNF-${\alpha}$ expression. TNF-${\alpha}$ mRNA stability analysis using reporter construct containing TNF-${\alpha}$ adenylate/uridylate-rich elements (AREs) shows that rapamycin destabilizes TNF-${\alpha}$ mRNA via regulating the AU-rich element of TNF-${\alpha}$ mRNA. The antigen-induced activation of S6K1 is inhibited by specific kinase inhibitors including mTOR, PI3K, PKC and $Ca^{2+}$chelator inhibitor, while TNF-${\alpha}$ mRNA level is reduced only by rapamycin treatment. These data suggest that the effects of rapamycin on the expression of TNF-${\alpha}$ mRNA are not mediated by S6K1 but regulated by mTOR. Taken together, our results reveal that mTOR signaling pathway is a novel regulation mechanism for antigen-induced TNF-${\alpha}$ expression in RBL-2H3 cells.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.39 no.9
• /
• pp.1263-1269
• /
• 2010

This study was performed to evaluate the antioxidant activities and anti-asthma effects of Morus bark water extracts. Inhibitory effect of Morus bark onto free radical generation was determined by measuring DPPH and hydroxyl radical scavenging activities in vitro. Anti-asthma activities of Morus bark water extracts were assessed by testing their effects on the degranulation of mast cell. For this, $\beta$-hexosaminidase released from a basophilic cell line, RBL-2H3 was used and pro-inflammatory cytokines were measured by ELISA kit. The antioxidant activities of water extracts of Morus bark was 59.2% in the DPPH assay at $2,000\;{\mu}g/mL$ and 78.8% in the hydroxyl radical scavenging assay at $2,000\;{\mu}g/mL$. Our results indicated that Morus bark water extracts effectively inhibited free radical generation. Morus bark water extracts inhibited inflammation-mediating substances such as histamine and $\beta$-hexosaminidase release from RBL-2H3 cells. Cytokine release demonstrated a more effective blockading ability of the Morus bark water extracts to the release of IL-4 and TNF-$\alpha$ compared to control. These results demonstrate that Morus bark may be beneficial in the treatment of allergic inflammatory disease.

• Applied Microscopy
• /
• v.41 no.3
• /
• pp.197-204
• /
• 2011

To investigate the alleviative effect of white tea water extract on the inflammation and skin barrier damage, skin aging animal model was produced by the irradiation of UVB to the backs of hairless mice for 12 weeks. And then experimental materials were applied topically for 4 weeks. At the 28th day of experiment, positive control (PC, 0.01% retinoic acid treatment) and experimental groups (E1, 1% white tea water extract treatment; E2, 2% white tea water extract treatment) had significantly (p<0.001) lower values of both skin erythema index and transepidermal water loss (TEWL) than the control (C, saline treatment) group. The appearance of mast cell and the degree of its degranulation in dermal and subcutaneous layers were remarkably reduced in E1 and E2 groups compared to the C group. It is found that white tea water extract is effective in skin barrier damage and inflammation in hairless mouse.

• Korean Journal of Clinical Laboratory Science
• /
• v.50 no.1
• /
• pp.37-43
• /
• 2018

Chamaecyparis obtusa (CO) has recently been attracting attention because of its beneficial effects on skin allergies, atopic dermatitis, and skin diseases, such as acne and eczema. In the present study, the extract from CO leaf grown in Jangseong gun, Jeollanam-do, Korea was evaluated for its anti-oxidant, anti-inflammatory, and anti-allergic effects in vitro. The total polyphenol content of the CO leaf extract was $25.89{\pm}0.31mg$ gallic acid equivalents (GAE)/g. Gas-chromatography mass-spectrometry (GC-MS) analysis revealed the presence of six compounds in the CO leaf extract: ${\alpha}-terpinene$ (3.03 mg/g), ${\alpha}-terpineol$ (9.48 mg/g), limonene (5.96 mg/g), borneol (59.78 mg/g), myrcene (4.85 mg/g), and sabinene (11.31 mg/g). The $RC_{50}$ values of the CO leaf extract for $H_2O_2$ and ABTS radical were $5.47{\pm}0.13mg/mL$ and $4.00{\pm}0.01mg/mL$, respectively. In addition, the CO leaf extract showed significant inhibitory effects on lipopolysaccharide-induced nitric oxide production in RAW 264.7 cells and IgE-induced release of ${\beta}-hexosaminidase$ (degranulation) in mast-cell like RBL-2H3 cells. The cell viability assay showed that the CO leaf extract ($100{\sim}800{\mu}g/mL$) did not affect the viability of human normal skin fibroblast CCD-986sk cells significantly. Overall, these results suggest that the CO leaf extract is a potential functional cosmetic ingredient that can exert anti-oxidant, anti-inflammatory, and anti-allergic effects.

• Applied Microscopy
• /
• v.38 no.4
• /
• pp.293-306
• /
• 2008

The essential factor of acute respiratory distress syndrome (ARDS), an acute lung injury accompanied commonly by sepsis syndrome is accumulation of neutrophils in lung tissue. The study attempted to confirm whether a lung injury would be decreased with the anti-inflammatory effect of germanium by the treated germanium prior to the development of ARDS and whether nitric oxide influence in suppressing a lung injury. Test groups were divided in the following structure for experiment; CON that has been administered with sodium chloride to airway, LPS administered with endotoxin for 5 hours in the same amount and 5 hours of endotoxin administered Ge+LPS following 1 hours of pre-treated germanium. The result of a test using experimental animals, infilteration of neutrophils (p<0.001) in bronchoalveolar lavage fluid (BALF) was significantly decreased, the structure of lung tissue was preserved relatively well, and much neutrophils with distinct positive were observed on tunel staining which showed increase of apoptotic neutrophils in the pre-treated germanium group compare to the endotoxin administrated group. In observation of ultrastructural changes of cell in BALF, phagocytic alveolar macrophage was increased in alveolar space, the nucleus of most engulfed neutrophils were condensed, and some apoptosis neutrophils appears to be DNA fragmentation and effacement of cellular organelles were found in intercellular matrix in the pre-treated germanium group. However, the nitric oxide showed increase in all the groups excluding CON, and the nitric oxide effect such as degranulation diminishing of mast cells and apoptosis increase of neutrophils in the pre-treated group only. The situation appears that there was change in internal environment of the experimental animal by the pre-treated germanium before the nitric oxide is produced and the anti-inflammatory effect activated the pre-processed germanium by nitric oxide which activated following the change. Therefore, the nitric oxide created from macrophage in accordance with the pre-treated germanium appears to influence in alleviating a lung injury. Accordingly, acute lung injury is alleviated by the anti-inflammatory effect of germanium such as inhibition of neutrophils migration, induction of neutrophil apoptosis and increase of phagocytic function of phagocyte, and the nitric oxide produced from activated macrophage by germanium would influence in suppressing a lung injury.