• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.13 no.2
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• pp.211-220
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• 2000

Shini-San has been used for treatment of allergic disease in Korea. However, its effect in experimental models remains unknown. The mast cell plays a pivotal role in initiating al1ergic response by secreting intracytoplasmic granular mediators such as histamine. The present report describes an inhibitory effect of Shini-San on mast cell-mediated immediate-type al1ergic reactions. Topical application of compound 48/80 can induce an ear swelling response in normal ($WBB6F_1-+/+$) mice but not in congenic mast cell-deficient $WBB6F_1-W/W^v$ mice. Shini-San inhibited concentration dependent mast cell-dependent ear swelling response induced by compound 48/80 in normal mice. Shini-San inhibited concentration-dependent passive cutaneous anaphylaxis induced by anti-dinitrophenyl (DNP) immunoglobulin E (IgE) in rats by topical application. Shini-San also inhibited in concentration-dependent fashion the histamine release from the rat peritoneal mast cells by compound 48/80 or anti-DNP IgE. Moreover, Shini-San had a significant inhibitory effect on compound 48/80-induced systemic anaphylactic reaction. These results indicate that Shini-San inhibits immediate-type allergic reactions by inhibition of mast cell degranulation in vivo and in vitro.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.244-244
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• 1994

Cortex Mori, the root bark of mulbery tree has been used as an antiphlogistic, diuretic, and expectorant in herbal medicine. The purpose of this study is to evaluate chicken gamma globulin (CGG)-specific IgE-induced morphologic and functional changes in rat peritoneal mast cells (RPMC), and to determine whether Cortex Mori could inhibit the CGG-specific IgE-depeildent mast cell degranulation and histamine release from RPMC. Results are 1) the degranuration and histamine release from RPMC were not induced within 1 hour after addition of Cortex Mori alone, 2) the CGG and CGG-specific IgE-Induced degranulation from RPMC was observed within 10 minutes, 3) the histamine release from RPMC sensitised with CGG-specific IgE was induced by tile addition of CGG, 4) CGG-specific IgE-dependent degranulation rate in RPMC pretreated with Cortex Mori was significantly Inhibited, compared to that of control group without Cortex Mori pretreatment, and 5) the CGG-specific IgE-dependent histamine release from RPMC was significantly inhibited by pretreatment with Cortex Mori. These data suggest that Cortex Mori contains some substances with capabilities to inhibit CGG-specific IgE-dependent degranulation and histamine release from RPMC.

• Advances in Traditional Medicine
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• v.2 no.2
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• pp.106-112
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• 2002

The effect of aqueous extract of Magnoliae Cortex (Magnoliaceae) (MCAE) on the immediate-type allergic reaction was investigated. MCAE inhibited compound 48/80 induced systemic anaphylactic reaction in rats. MCAE (0.1 and 1 g/kg) also significantly inhibited local immunoglobulin E (lgE)-mediated passive cutaneous anaphylactic (PCA) reaction. MCAE (0.001 to 1 mg/ml) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-dinitrophenyl (DNP) 1gE. Moreover, MCAE (0.01 to 1 mg/ml) had a significant inhibitory effect on anti-DNP IgE-mediated tumor necrosis $factor-{\alpha}$ $(TNF-{\alpha})$ production. These results indicate that MCAE inhibits immediate-type allergic reaction in vivo and in vitro.

• Natural Product Sciences
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• v.7 no.4
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• pp.95-101
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• 2001

We investigated the effect of aqueous extract of Terminalia chebula (Combretaceae)(TCAE) on the immediate hypersensitivity reaction in vivo and in vivo. TCAE (0.01 to 1 g/kg) dose-dependently inhibited compound 48/80 induced systemic anaphylaxis in mice. When TCAE was pretreated at concentrations ranging from 0.01 to 1 g/kg, the plasma histamine levels were reduced in a dose-dependent manner. TCAE (0.1 and 1 g/kg) significantly inhibited local immunoglobulin E (IgE)-mediated passive cutaneous anaphylactic reaction. TCAE (0.001 to 1 mg/ml) also dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-dinitrophenyl (DNP) IgE. TCAE (0.01 to 1 mg/ml) had a significant inhibitory effect on anti-DNP IgE-induced tumor necrosis $factor-{\alpha}$ production from RPMC. These results indicate that TCAE inhibits immediate hypersensitivity reaction in vivo and in vitro.

• Archives of Pharmacal Research
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• v.22 no.6
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• pp.642-645
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• 1999

In a bioassay-guided search for anti-allergic compounds from higher plants of Korea, poly-methoxyflavones, 3',4',5,6,7,8-hexamethoxyflavone (I), 5-hydroxy-3',4',6,7,8-pentamethoxyflavone (II) and 3',4',5,7,8-pentamethoxyflavone (III) have been isolated from the immature peels of Citrus unshiu. Structures of these compounds were elucidated on the basis of spectroscopic techniques. Compounds I and II inhibited dose-dependent histamine release from the rat peritoneal mast cells activated by compound 48/80 or anti-DNP IgE.

• Advances in Traditional Medicine
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• v.2 no.1
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• pp.58-63
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• 2002

The effect of the aqueous extract of Rubus coreanus Miq. (Rosaceae) fruits (AERC) on anaphylactic reaction was investigated. AERC completely inhibited compound 48/80-induced systemic anaphylactic shock at dose of 0.1 to 1.0 g/kg. When AERC was pretreated at concentrations ranging from 0.01 to 1.0 g/kg, the plasma histamine levels induced by compound 48/80 were reduced in a dose-dependent manner. AERC also inhibited the histamine release from rat peritoneal mast cells (RPMC) by compound 48/80. The level of cAMP in RPMC, when AERC (1.0 mg/ml) was added, transiently and significantly increased about 6-fold compared with that of basal cells. These results indicate that AERC may be beneficial in the treatment of non-specific anaphylactic reactions.

• Natural Product Sciences
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• v.9 no.1
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• pp.44-48
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• 2003

The effect of aqueous extract of Stachys riederi var. japonica Miq. (Labiatae) (SRAE) on the immediate-type allergic reactions was investigated. SRAE was found to exhibit a inhibitory activity on the compound 48/80-induced systemic anaphylaxis in mice. SRAE inhibited the plasma histamine release induced by compound 48/80 in mice. In addition, SRAE also inhibited the passive cutaneous anaphylaxis reaction induced by IgE/anti-IgE in mice. The effect of SRAE on the histamine release from rat peritoneal mast cells (RPMC) was studied. SRAE inhibited the histamine release induced by compound 48/80 in RPMC. To clarify the mechanism of these inhibiting reactions, we investigated the effects of SRAE on cyclic AMP (cAMP). The level of cAMP in human leukemia cell line, HMC-1, when SRAE (1 mg/ml) was added, significantly increased compared with that of basal cells. These results indicate that SRAE may be beneficial in the treatment of immediate-type allergic reaction.

• Natural Product Sciences
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• v.8 no.4
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• pp.177-182
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• 2002

The effect of aqueous extract of Sanguisorba officinalis L. (Rosaceae) root (SOAE) on the immediate-type allergic reactions by anal therapy was investigated. SOAE (0.01 to 1 g/kg) dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in mice. When SOAE was pretreated at the same concentrations with systemic anaphylaxis, the plasma histamine levels were reduced in a dose-dependent manner. SOAE (0.1 and 1 g/kg) also significantly inhibited local anaphylaxis activated by anti-DNP IgE. SOAE (0.001 to 1 mg/ml) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cyclic AMP (cAMP) in RPMC, when SOAE (1 mg/ml) was added, transiently and significantly increased compared with that of basal cells. These results provide evidence that anal therapy of SOAE may be beneficial in the treatment of allergic diseases.

• Advances in Traditional Medicine
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• v.3 no.2
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• pp.56-62
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• 2003

The effect of aqueous extract of Terminalia chebula fruit (Combretaceae) (TCAE) by anal administration on mast cell-dependent immediate-type anaphylactic reactions was investigated. TCAE (0.005 to 1 g/kg) inhibited systemic anaphylaxis induced by compound 48/80 in mice. When TCAE was pretreated at the same concentrations with systemic anaphylaxis, the plasma histamine levels were reduced in a dose-dependent manner. TCAE (0.1 and 1 g/kg) also significantly inhibited local anaphylaxis activated by anti-DNP IgE. TCAE (0.001 to 1 mg/ml) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. Moreover, TCAE (0.01 and 0.1 mg/ml) had a significant inhibitory effect on anti-DNP IgE-mediated tumor necrosis $factor-{\alpha}$ $(TNF-{\alpha})$ production from RPMC. These results provide evidence that anal therapy of TCAE may be beneficial in the treatment of systemic and local mast cell-dependent anaphylaxis.

• Korean Journal of Pharmacognosy
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• v.30 no.4
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• pp.377-383
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• 1999

The anti-asthmatic activities of the extract of Lonicera japonica (BuOH fraction) and its mode of action were investigated using several in vitro and in vivo models. Lonicera japonica was extracted with 30% ethanol (v/v) and successively partitioned into BuOH. The BuOH fraction reduced antigen-induced contraction of isolated trachea from sensitized guinea pigs in a concentration-dependent manner. The BuOH fraction also inhibited histamine release from rat peritoneal mast cells induced by antigen or calcium ionophore A23187 ($IC_{50}=0.26$ and 0.32mg/ml, respectively). Eosinophil infiltration into bronchoalveolar lavage fluids induced by aeroallergen challenge in passively sensitized guinea pigs was inhibited by the BuOH fraction at a dose of 800mg/kg (51.7%). In addition, the BuOH fraction inhibited leukotriene $B_4$ prodution in rat basophilic leukemia cells ($IC_{50}=0.42\;mg/ml$) as well as phosphodiesterase 4 (PDE4) isolated from rat brain ($IC_{50}=0.015\;mg/ml$). All results from this study strongly suggest that the BuOH fraction of Lonicera japonica may be useful in the treatment of asthma and its mode of action may be related with inhibition of both 5-lipoxygenase and PDE4 enzyme.