• Journal of Life Science
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• v.21 no.12
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• pp.1721-1725
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• 2011

Mast cells are major effector cells associated with allergic responses. They are activated through the release of histamine, arachidonic acid, and proinflammatory cytokines. We investigated the effect of nodakenin, derived from the roots of Angelica gigas Nakai, on mast cell degranulation and on an allergic response in an animal model. We also investigated the effect of nodakenin on expression of multiple cytokines. Nodakenin suppressed the release of ${\beta}$-hexosaminidase, a marker of degranulation, as well as the expression of interleukin IL-4 and TNF-${\alpha}$ mRNA. Nodakenin inhibited the passive cutaneous anaphylaxis (PCA) reaction in ICR mice in a dose-dependent manner. These results suggest that nodakenin can inhibit mast cell degranulation through the inhibition of IL-4 and TNF-${\alpha}$ mRNA expression, and that nodakenin may potentially serve as an anti-allergic agent.

• Journal of Life Science
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• v.22 no.5
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• pp.595-599
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• 2012

Allergic response is associated with mast cells, through the release of arachidonic acid, proinflammatory cytokines, and histamine. We investigated the effect of Platycodon grandiflorum including platycodin D (PG-Platycodin D) on allergic responses in an animal model and on mast cell degranulation. PG-Platycodin D suppressed the release of ${\beta}$-hexosaminidase, a type of marker associated with degranulation. PG-Platycodin D efficiently inhibited the passive cutaneous anaphylaxis (PCA) reaction in ICR mice. In addition, molecular analysis demonstrated that PG-Platycodin D inhibited mRNA expression of both IL-3. These results suggest that PG-Platycodin D can inhibit mast cell degranulation through the inhibition of IL-3 mRNA expression, and that PG-Platycodin D may potentially serve as an anti-allergic agent.

• The Journal of Dong Guk Oriental Medicine
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• v.6 no.1
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• pp.117-128
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• 1997

Abdominal skin tissues of ICR mouse painted with Dinitrochlorobenzene (DNCB) were observed to investigate the delayed type hypersensitivity of skin by chemical allergen as hapten. The abdominal skin tissues were obtained at hour 48 after secondary DNCB sensitization that were stained by Luna's method for mast cell, and immunohistochemical stain method for IL-2 receptor. The superficial perivascular lymphocytic aggregation were shown in basement membrane after DNCB secondary painting and the large size capillaries in dermis were appeared. The infiltration of lymphocyte to epithelium, the vacuolation of epithelial cell and intercellular space were increased. The number of mast cell in dermis was increased and these shape is degranulation type. The number of IL-2 receptor positive cell was increased in dermis. As results indicated that the hypersensitivy of immune system were induced by DNCB, subsequently to damage evoke inflammation in skin.

• The Korean Journal of Pharmacology
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• v.30 no.2
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• pp.243-254
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• 1994

Inflammatory diseases, allergic and asthmatic disorders are caused by the mediator release from the activation of the phospholipase C (PLC), phospholipase D (PLD), methyltransferase or adenylate cyclase etc. during IgG or IgE cross-linking of high affinity receptors on mast cells or basophil surface. One important enzyme activated after IgG or IgE receptor cross-linking is PLD, the enzyme which converts phosphatidylcholine (PC) to phosphatidic acid (PA). Under the hypothesis that these may be some differences in mediator release according to the difference in PLD activity, we attempted to confirm the ginseng saponin effects on the PLD activity. We examined the PLD activity during the passively sensitized mast cell activation in the presence of single component of ginsenosides $(Rc,\;Rg_1,\;Rg_2,\;Rg_3)$. We also measured the amount of mediators (histamine and leukotrienes) released by stimulating with ovalbumin (OA) or calcium ionophore (CaI), Guinea Pig lung mast cells were purified using enzyme digestion, count current elutriation, and discontinuous Percoll density gradient. In purified mast cells prelabeled with $[^3H]$ arachidonic acid or $[^3H]$ palmitic acid, PLD activity was assessed more directly by the production of labeled PEt by PLD-mediated transphosphatidylation in the presence of ethanol. Histanine release was determined by Spectrophotofluorometry, and leukotrienes by radioimmunoassay. The PLD activity during the passively sensitized mast cell activation is increased up to $3{\sim}5times$. The PLD activity during the passively sensitized mast cell activation in the presence of all ginsenosides is decreased up to $4{\sim}11$ times. $Rg_l\;and\;Rg_2$ ginsenoside pretreatment decreased histamine and leukotrienes by 50% in the OA-induced or by 40% in the Cal-induced mast cell after passively sensitization. Rc pretreatment poorly decreased histamine but leukotrienes decreased by 70% in the OA-induced or by 35% in the Cal-induced mast cell. $Rg_3$ ginsenoside pretreatment increased histamine release without challenging OA or Cal but leukotrienes decreased. These observations indicate that single unit of ginsenosldes may be an important contributor to inhibit the release of histamine and leukotrienes in the guinea pig lung mast cells, that inhibits the PLD-mediated formation of DAG evoked by mast cell activation.

• Journal of Life Science
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• v.21 no.10
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• pp.1364-1369
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• 2011

Mast cells, the central effector cells involved in the allergic response, release histamine, arachidonic acid, and proinflammatory cytokines. We investigated the effect of the ethyl acetate fraction (EA), derived from Korean rice wine lees, on RBL-2H3 cell degranulation and passive cutaneous anaphylaxis in an animal model. The EA fraction suppressed the release of beta-hexosaminidase, a marker of degranulation, and the mRNA expression of interleukin-3 (IL-3) and IL-13. EA also successfully suppressed the passive cutaneous anaphylaxis (PCA) reaction in mice in a dose-dependent manner. These results suggest that EA can inhibit mast cell degranulation through the inhibition of IL-3 and IL-13 mRNA expression, and that EA may potentially serve as an anti-allergic agent.

• Journal of Digital Convergence
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• v.13 no.1
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• pp.341-351
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• 2015

This study was aimed to evaluate the effects of Cypress oil(CS) on anti-asthmatic activities in a mouse model of allergic asthma. Using an Ovalbumin-induced allergic asthma mouse model, 0.3% of CS was administered to experimental group using a nebulizer for 3 weeks on a basis of 3 times per week and 30min each time. The degree of airway hypersensitivity, the number of eosinophil in white blood cells, the number of immune cells and the change of cytokine in lung tissue were evaluated. The degree of airway hypersensitivity, the number of eosinophil, IL-5 and IL-13 levels in lung tissue, IgE in serum, the number of CCR3, CD3, CD4 cells were significantly decreased in experimental group treated with CS. These results suggested that CS may have a positive effects on Th2 cytokine and eosinophils which are major factors of asthma responses. Therefore CS might be of therapeutic value in treating asthma.

• Microbiology and Biotechnology Letters
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• v.36 no.4
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• pp.343-352
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• 2008

Frankincense, the gum resin derived from Boswellia species, is complex mixtures composed of about $5{\sim}9%$ highly aromatic essential oil, $65{\sim}85%$ alcohol-soluble resins, and the remaining water-soluble gums. The anti-inflammatory properties of frankincense, alcohole-soluble resins, are well-recognized, but the question of whether aromatic essential oil also plays a role in the allergic asthma remains unanswered. This study was performed to evaluate anti-inflammatory effects of Boswellia sacra essential oil (BSEO) on ovalbumin (OVA)-induced asthma mouse model. BALB/c mice after intraperitoneal OVA sensitization were challenged with intratracheal OVA. One experimental group was inhaled with 0.3% BSEO for the later 8 weeks. BALB/c mice were sensitized and challenged with OVA and developed airway eosinophilia, mucus hypersecretion, and airway hyperresponsiveness. In contrast, the BSEO treated mice had reduced a number of eosinophils among BALF cells, goblet cell hyperplasia, and airway hyperresponsiveness. Cytokine analysis of BALF revealed that BSEO caused an increase in Th1 cytokine (interferon-$\gamma$ (IFN-$\gamma$)) and a decrease in Th2 cytokines (interleukin-4 (IL-4), IL-5 and IL-13) levels. In addition, the OVA-specific serum IgE and eotaxin levels were also reduced. In mice inhaled BSEO, $CD4^+$, $CD3^+/CCR3^+$, and $B220^+/CD23^+$ mediastinal lymph nodes cells were also decreased. These results suggest that inhaled BSEO as a immunomodulator in Th1/Th2 mediated asthma may have therapeutic potential for the treatment in allergic airway inflammation by a simple, cost-effective way.

• The Journal of Dong Guk Oriental Medicine
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• v.8 no.1
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• pp.77-91
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• 1999

After allergic contact dermatitis elicitated by Dinitrochlorobenzene(DNCB) treatment, ICR female mice administered Yunkyopaedocksangamibang(YPGM) extract were observed to investigate the effect of YPGM on allergic contact dermatitis. This study investigated that contact hypersensitivity assay, abdominal skin morphologic changes including mast cells. At contact hypersensitivity assay, the right ear swelling in YPGM group were probability decreased than DNCB group. At observation of abdominal skin morphologic change, the infiltration of lymphocyte, lymphocyte insertion to epithelium, enlarged capillary, angiogenesis, and damages of epithelium as cytoplasmic vacuolation and enlarge of inter cellular space in YPGM were diminished than DNCB group. The number of mast cell was increased both DNCB and YPGM group. The shape of mast cell in DNCB group was mainly appeared degranulated type, but granulated type in YPGM group. The number of serotonin positive cell was increased both DNCB and YPGM group. The shape of serotonin positive cell in DNCB group was mainly appeared degranulated type, but granulated type in YPGM group. As results indicated that the YPGM extract administration work on the mitigation of skin damages in mouse with allergic contact dermatitis.

• Microbiology and Biotechnology Letters
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• v.38 no.1
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• pp.93-104
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• 2010

In this study, we investigated the effects of frankincense essential oil (BSEO) on the immune cell change in the lung, BALF and PBMC using a mouse model of asthma. BALB/c mice after intraperitoneal OVA sensitization (day 1) were challenged intratracheally with OVA on day 14. Then, the asthma was induced by repeated OVA inhalation challenged. The asthma induced mice group inhaled 0.3% BSEO for 30 minutes per trial, three times a week, for 8 weeks using the nebulizer. After 12 weeks from the experiment, the mice was killed and the lung, bronchoalveolar lavage fluid (BALF) and peripheral blood mononuclear cell (PBMC) were obtained. Next, the change of immune cells inside the separated tissues was observed to identity the effects of BSEO on the allergic asthma mice. In conclusion, the hypersensitive reaction of airway to the bronchoconstrictor in the allergic asthma induced mice was effectively suppressed in Frankincense group, in Bermagot, Eucalyptus, Chamomile, Marjoram and Frankincense groups, the natural aromatic essential oil groups. Furthermore, it was also confirmed that the weight of lung, total number of alveolus cells and the number of BALF, MNL and DLN increased after inducing allergic asthma were reduced. BSEO suppressed the percentage of $CD3e^+/CD19^-$, $B220^+/CD23^+$ and $CD11b^+/Gr-1^+$ cells in the lung tissue of allergic asthma mice. Moreover, BSEO also reduced the percentage of $CD4^+/CD8^-$, $B220^+/CD23^+$ and $CD3^+/CCR3^+$ cells in BALF. In addition, the percentage of $CD3e^+/CD19^-$, $CD3^+/CD69^+$ and $B220^+/CD23^+$ cells in PBMC was reduced. The results of this study indicate that BSEO would be effective to treat allergic asthma by the immune control suppressing the activity of immune cells in each tissue.