• Journal of Acupuncture Research
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• v.23 no.5
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• pp.167-175
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• 2006

Objectives : We studied the effects of Radix Asteris herbal acupuncture solution (RAHAS) on the type I hypersensitivity. Methods : In vivo, we measured compound 48/80 induced active systemic anaphylactic shock, anti-DNP IgE induced passive cutaneous anaphylaxis (PCA) and acetic acid induced microvascular permeability using ICR mice. In vitro, we showed effects on cytotoxicity and ${\beta}$-hexosaminidase release from RBL-2H3 cells. Results : In vivo, RAHAS pretreatments at $BL_{13}$ and optional points inhibited active systemic anaphylactic shock induced by compound 48/80 and microvascular permeability increased by acetic acid. PCA was only inhibited by RAHAS pretreatments at $BL_{13}$. In vitro, RAHAS treatments inhibited ${\beta}$-hexosaminidase release. Conclusion : These results suggest that RAHAS may be beneficial in the prevention of type I hypersensitive inflammatory response.

• Korean Journal of Acupuncture
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• v.23 no.3
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• pp.111-122
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• 2006

Objectives : We studied the effects of Scutellariae Radix pharmacopuncture solution (SRHAS) on the type 1 hypersensitivity. Methods : In vivo, we measured compound 48/80-induced active systemic anaphylactic shock using ICR mice and anti-DNP IgE-induced passive cutaneous anaphylaxis (PCA) using Sprague Dawley rats. In vitro, we showed effects on cytotoxicity and ${\beta}-hexosaminidase$ release from RBL-2H3 cells. Results : In vivo, SRHAS pretreatments (100% or 50%) at BL13 inhibited active systemic anaphylactic shock induced by compound 48/80. PCA was only inhibited by pretreatments of SRHAS at optional points. In vitro, $0.1{\sim}2%$ SRHAS treatments did not affect cell viability while ${\beta}$-hexosaminidase release was significantly inhibited. Conclusions : These results suggest that SRHAS may be beneficial in the inhibition of type I hypersensitive inflammatory response.

• Korean Journal of Pharmacognosy
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• v.43 no.3
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• pp.243-249
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• 2012

Bee venom (BV), well known as a traditional Oriental medicine, has been widely used in the treatment of some immune-related diseases. However, the anti-allergic effect of BV have not been reported. In this study, we investigated the antiallergic effect of BV on triphasic cutaneous reaction (TpCR) and passive cutaneous anaphylaxis (PCA). Our results indicated that BV suppress ear swelling and vascular permeability on IgE mediated type I hypersensitivity response. Increase in ear thickness was significantly inhibited by BV in this model. BV also blocked the infiltration of immune cells into the ear. Moreover, BV suppressed expression of HDAC3, Tryptase, MCP-1 in ear tissue. These results demonstrated that BV has a suppressive effect on allergic reaction.

• Journal of Korean Academy of Nursing
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• v.23 no.4
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• pp.528-543
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• 1993

Vitamin E, which has its advocates in the treatment of diabetes mellitus. autoimmune disease, cancer and peripheral vascular and thromboembolic disease, has now been alleged to have a powerful antioxident effect and to affect various biological activities such as fertility factor, inhibition of human platelet aggregation and stabilization of biological membranes. The present study was designed to test whether vitamin I(alpha-tocopherol) can : (1) enhance the hemagglutinin response to sheep red blood cells (SRBC), (2) modulate Arthus and delayed type hypersensitivity(DTH) to SRBC and contact hypersensitivity to dinitrofluorobenzene (DNFB). (3) enhance the mitogenic response of murine splenocyte, (4) decrease the recovery of Cryptococcus neoformans from brain, lung, liver, spleen and kidney of infected mice and (5) have an inhibitory or enhancing effect on the induction of active systemic anaphylaxis(ASA) induced by chicken-gamma globulin (CGG) in mice. Mice were given either intramuscular injections of 0.3ml (300mg) of vitamin I before immunization or were infection for 10 consecutive days or were given by vitamin I esophageal intubation, 0.1ml(100mg), for 20 days before sacrifice for the mitogenic response experiments. It was found that vitamin E treated mice showed a significant enhancement in hemagglutinin response, Arthus reaction and DTH to SRBC and contact hypersensitivity to DNFB. There was no significant difference in the mitogenic response to phytohemagglutinin(PHA), but the response to concanavalin A(ConA) or pokeweed mitogem(PWM) was increased in vitamin E-treated mice. Interestingly, the vitamin E administration before C. neoformans infection decreased significantly the recovery of C. neoformans from brain lung, liver, spleen and kidney of the infected mice as compared with that of the control mice, strongly suggesting that vitamin E pretreatment may increase the resistance of mice to the fungal infection. Unexpectedly, vitamin E administration enhanced the production of CGG -induced ASA. Taken together, it can be concluded that vitamin I administration may in-crease the humoral and cellular immune response and resistance. to C. neoformans infection, but enhance the induction of ASA to CGG. Further studies are necessary to clarify the underlying mechanism accounting for these effects.

• Korean Journal of Pharmacognosy
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• v.14 no.3
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• pp.102-106
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• 1983

As many crude drugs are used in the oriental medical field problems on the side effects of these drugs come to the front. To conduct delayed-type hypersensitivity we selected 29 kinds of drugs used frequently for therapeutic agents in oriental medical hospitals (Table I). The cell-mediated immune response was evaluated by measuring the foot pad swelling reaction and humoral immune response by measuring the antibody formation to these crude drugs. Mice were given these drugs intraperioneally for sensitization and challenged with same drug as used for sensitization respectively by intral dermal injection on the left and righ hind foot pad 4 days after senstization and then the foot pads were measured with the dial micrometer. The results were as follow; 1) Gentianae Scabrae Radix, Arecae Semen, Corydalis Tuber, and Paeoniae Radix were significant as delayed-type hypersensitivity inducers. 2) None of the crude drugs tested had effect on the induction of humoral immune response.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.4 no.1
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• pp.1-22
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• 1991

The object of this research is to find out the clinical effects of Sopungsan and Gamisopungsan on Immune response and the An1i-allergic reaction to rats and mice. The results obtained are as follows: 1. Both sopungsan and Gamisopungsan have a tendency to decrease on the delayed type hypersensitivity response in methotrexate treated mice, but are not recognized as having significance. 2. Both Sopungsan and Gamisopungsan reveal the increasing effects with significance on the hemagglution titer in mice. 3. Gamisopungsan reveals the increasing effect with significance on the hemolysin titer in mice. 4. Both Sopungsan and Gamisopungsan have a tendency to increase on the appearance of Rosette forming cells in mice, but are not recognized as having significance. 5. Both Sopungsan and Gamisopungsan reveal the increasing effects with significance on phagocytic index K and a in mice 6. Sopungsan reveals the decreasing effect, on the homologous passive cutaneous anaphylaxis in rats provoked by the IgE-like antibody aganist egg white albumin. 7. Gamisopungsan reveals the decreasing effect with significance on vascular permeabi1ity response to intradermal histamin in rats. 8. Sopungsan reveals the decreasing effect with significance, on vascular permeability response to intradermal serotonin in rats. 9. Both Sopungsan and Gamisopungsan reveal the decreasing effects with significance on the delayed type hypersensitivity response to picryl chloride in mice. 10. Both Sopungsan and Gamisopungsan reveal the decreasing effects with significance on the delayed type hypersensitivity response to sheep red blood cell in mice. According to the above results, Sopungsan and Gamisopungsan are concluded to have the increasing effect of immunity and anti-allergic reaction.

• The Journal of Pediatrics of Korean Medicine
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• v.8 no.1
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• pp.27-37
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• 1994

This Experimental study was done to investigate the effect of the Taklisodok-um on the Anti-allergic response. The results were obtained as follows: 1. On vascular permeability response to the intradermal injected Histamine, the Taklisodok-um treated group revealed more significant decrease than control group. 2. On vascular permeability response to the intradermal injected Serotonin, the Taklisodok-um treated group revealed more significant decrease than control group. 3. In the 48hrs homologous passive cutaneous anaphylaxis provoked by the IgE-like antibody against white egg albumin, there was no significant difference between the Taklisodok-um treated group and control group. 4. The Taklisodok-um treated group revealed more significant inhibitory effect than control group in the delayed type hypersensitivity response to Picryl chloride. 5. The Taklisodok-um treated group revealed more significant inhibitory effect than control group in the delayed type hypersensitivity response to SRBC. According to the above-stated results, it is considered that the Taklisodok-um could be applied widely to the type I and IV allergic diseases.

• Biomolecules & Therapeutics
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• v.28 no.5
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• pp.456-464
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• 2020

Mast cells (MCs) are systemically distributed and secrete several allergic mediators such as histamine and leukotrienes to cause type I hypersensitivity. Dasatinib is a type of anti-cancer agent and it has also been reported to inhibit human basophils. However, dasatinib has not been reported for its inhibitory effects on MCs or type I hypersensitivity in mice. In this study, we examined the inhibitory effect of dasatinib on MCs and MC-mediated allergic response in vitro and in vivo. In vitro, dasatinib inhibited the degranulation of MCs by antigen stimulation in a dose-dependent manner (IC₅₀, ~34 nM for RBL-2H3 cells; ~52 nM for BMMCs) without any cytotoxicity. It also suppressed the secretion of inflammatory cytokines IL-4 and TNF-α by antigen stimulation. Furthermore, dasatinib inhibited MC-mediated passive cutaneous anaphylaxis (PCA) in mice (ED₅₀, ~29 mg/kg). Notably, dasatinib significantly suppressed the degranulation of MCs in the ear tissue. As the mechanism of its effect, dasatinib inhibited the activation of Syk and Syk-mediated downstream signaling proteins, LAT, PLCγ1, and three typical MAP kinases (Erk1/2, JNK, and p38), which are essential for the activation of MCs. Interestingly, in vitro tyrosine kinase assay, dasatinib directly inhibited the activities of Lyn and Fyn, the upstream tyrosine kinases of Syk in MCs. Taken together, dasatinib suppresses MCs and PCA in vitro and in vivo through the inhibition of Lyn and Fyn Src-family kinases. Therefore, we suggest the possibility of repositioning the anti-cancer drug dasatinib as a treatment for various MC-mediated type I hypersensitive diseases.

• Biomolecules & Therapeutics
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• v.30 no.6
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• pp.520-528
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• 2022

Mast cells are an effector cell that plays a pivotal role in type I hypersensitive immune responses. Mast cells exist in connective tissues, such as skin and mucosal tissue, and contain granules which contain bioactive substances such as histamine and heparin in cells. The granules of mast cells are secreted by antigen stimulation to cause the type I allergic hypersensitivity. In addition, stimulated by antigen, mast cells synthesize and secrete various eicosanoids and cytokines. While AT9283 is known to have anticancer effects, the therapeutic effect of AT9283 on allergic disorders is completely unknown. In this study, it was found that AT9283 reversibly inhibited antigen-IgE binding-induced degranulation in mast cells (IC₅₀, approx. 0.58 μM) and suppressed the secretion of the inflammatory cytokines IL-4 (IC₅₀, approx. 0.09 μM) and TNF-α (IC₅₀, approx. 0.19 μM). For a mechanism of mast cell inhibition, while not inhibiting Syk phosphorylation, AT9283 suppressed the activation of LAT, a downstream substrate protein of Syk, in a dose-dependent manner. As expected, AT9283 also inhibited the activation of PLCγ1 and Akt, downstream signaling molecules of Syk/LAT, and MAP kinases such as JNK, Erk1/2, and P38. In an in vitro protein tyrosine kinase assay, AT9283 directly inhibited Syk activity. Next, AT9283 dose-dependently inhibited passive cutaneous anaphylaxis (PCA), an IgE-mediated allergic acute response, in mice (ED50, approx. 34 mg/kg, p.o.). These findings suggest that AT9283 has potential to use as a new drug for alleviating the symptoms of IgE-mediated allergic disorders.

• YAKHAK HOEJI
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• v.42 no.1
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• pp.75-81
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• 1998

Effects of swainsonine (SW: 8${\alpha}$, ${\beta}$-indolizidine-1alpha, 2${\alpha}$, 8${\beta}$-triol from Locoweed) on the cellular and nonspecific immune responses of lipopolysaccharide (LPS) wer e studied in ICR mice. Mice were divided into 4 groups (10mice/group), and LPS was given to each mouse 1 hr after i.p. injection with 3.7mg/kg of SW by i.p. injection twice a week for 14 days at a dose of 2mg/kg. Immune responses of the delayed-type hypersensitivity response (DTH) to sheep red blood cells (s-RBC), phagocytic activity and natural killer (NK) cell activity were evaluated. LPS treatment didn`t affect NK cell activity, phagocytic activity, DTH to s-RBC compared with those in controls, and phagocytic activity of sareoma 180 tumor bearing mice. However, circulating leukocytes were significantly decreased. Combinaton of LPS and SW increased circulating leukocytes significantly compared vath that in LPS alone, and DTH to s-RBC, NK cell activity and phagocytic activities of normal and sarcoma tumor bearing mice were not affected. These findings indicate that SW didn`t affected the cellular immune responses suppressed by LPS but significantly increased circulating leukocytes.