Effect of Lo Han Kuo (Siraitia grosvenori Swingle) on nasal rubbing and scratching behavior in ICR mice

We studied the effect of Lo Han Kuo (Siraitia grosvenori Swingle) on histamine-induced nasal rubbing and compound 48/80-induced skin scratching behavior in ICR mice. An extract and glycoside (a complex of sweet components) of Lo Han Kuo were used in the study. Both the extract and glycoside caused no significant effect on nasal rubbing or scratching behavior, even at a dose of 1000 mg/kg when administered in a single dose. However, the effect of Lo Han Kuo became clear after repeated administration, and 300 and 1000 mg/kg of both extract and glycoside significantly inhibited nasal rubbing and skin scratching behavior after consecutive treatment for 4 weeks. Both the extract and glycoside inhibited the histamine release induced by compound 48/80 at concentrations of 300 and 1000 microg/ml. From these results, it is assumed that the inhibition of nasal rubbing and skin scratching behavior induced by Lo Han Kuo occurs through a mast cell-dependent mechanism.     

Antipruritic and antierythema effects of ascomycete Bulgaria inquinans extract in ICR Mice

The effect of ethanol extract obtained from Bulgaria inquinans on the scratching behavior and vascular permeability changes induced by compound 48/80, histamine and serotonin in ICR mice was studied. The extract dose-dependently inhibited scratching behavior induced by compound 48/80 and serotonin. A significant inhibition was observed at doses of 300 and 600 mg/kg when Bulgaria inquinans extract was administered orally. However, no inhibitory effect was observed on the histamine-induced scratching behavior by the extract, even at a dose of 600 mg/kg. In addition, it also inhibited the increase in the vascular permeability induced by compound 48/80 and serotonin at doses of 300 and 600 mg/kg; however, it failed to inhibit the increased vascular permeability induced by histamine, even at a dose of 600 mg/kg. Bulgaria inquinans extract showed a potent inhibitory effect on histamine release induced by compound 48/80. These results suggest that Bulgaria inquinans extract is effective in cutaneous pruritus and erythema, which were probably mediated by inhibiting the release of histamine from mast cells and antagonizing the effect on serotonin.     

Caffeic acid inhibits compound 48/80-induced allergic symptoms in mice

The effect of caffeic acid on scratching behavior and vascular permeability changes induced by compound 48/80 in ICR mice were investigated. An oral dose of 500 mg/kg of caffeic acid significantly inhibited scratching behavior and vascular permeability induced by compound 48/80. The inhibitory effects of daily administration of lower doses of caffeic acid, 100 and 200 mg/kg, were also investigated; and it was found that 200 mg/kg significantly inhibited compound 48/80-induced scratching behavior after the second week of consecutive administration. The effect of 200 mg/kg of caffeic acid on scratching behavior was observed up to the third week of the treatment. The decrease in histamine content induced by compound 48/80 was significantly antagonized by 200 mg/kg. The findings suggest that caffeic acid may be effective for treating itch and edema in allergic dermatitis.     

Antipruritic and antiinflammatory effects of aqueous extract from Si-Wu-Tang

Si-Wu-Tang (SWT), a traditional Chinese formula, has been clinically used in the treatment of cutaneous pruritus, chronic inflammation, and other diseases. The present study was carried out to observe the antipruritic and antiinflammatory effects of SWT aqueous extract using compound 48/80 and picryl chloride (PC) models in mice. SWT (500, 1000 mg/kg p.o.) clearly reduced the scratching responses elicited by compound 48/80 in normal mice. At doses of 250 and 500 mg/kg, it inhibited the scratching responses induced by PC in mice actively sensitized with 2,4-dinitrophenol (DNP)-ovalbumin (OVA) plus alum. Furthermore, SWT (250, 500, 1000 mg/kg) significantly inhibited the footpad swelling caused by compound 48/80 in mice. In the biphasic ear skin reactions induced by PC in actively sensitized mice, SWT (250, 500 mg/kg) reduced the immediate-phase reaction, but did not affect the late-phase reaction. In vitro, SWT (50-500 microg/ml) showed a concentration-dependent inhibition of the histamine release induced by compound 48/80 from rat peritoneal mast cells. The crude drugs contained in SWT, Paeoniae Radix (25, 100 microg/ml), Rehmanniae Radix, and Chuanxiong Rhizoma (100 microg/ml), also showed a clear inhibition, but Angelica Radix did not at the concentrations examined. These findings indicate that SWT aqueous extract has antipruritic and antiinflammatory effects in mice. SWT inhibits histamine release from rat mast cells, and Paeoniae Radix probably plays a crucial role in the formula.     

Participation of histamine H1 and H2 receptors in passive cutaneous anaphylaxis-induced scratching behavior in ICR mice

Scratching behavior associated with passive cutaneous anaphylaxis was examined and compared to that induced by compound 48/80 or histamine in ICR mice. Elicitation of passive cutaneous anaphylaxis, and intradermal injections of compound 48/80, histamine or serotonin induced both scratching behavior and vascular permeability increase in ICR mice. In mast cell-deficient WBB6F1-W/Wv mice, although histamine induced scratching behavior and vascular permeability increase, passive cutaneous anaphylaxis was not observed. Cetirizine and terfenadine significantly inhibited the scratching behavior and vascular permeability increase caused by passive cutaneous anaphylaxis, compound 48/80 and histamine. The histamine H1 receptor antagonists inhibited the vascular permeability increase almost completely, whereas they failed to abolish the scratching behavior. Famotidine and ranitidine significantly inhibited the scratching behavior caused by histamine. The histamine H2 receptor antagonists did not affect the vascular permeability increase caused by histamine. The combination of cetirizine and ranitidine abolished the histamine-induced scratching behavior. The combination, however, failed to potentiate the inhibition of passive cutaneous anaphylaxis-induced scratching behavior significantly. The results indicated that histamine induces scratching behavior in ICR mice through both histamine H1 and H2 receptors, and that histamine plays a major role in passive cutaneous anaphylaxis-induced scratching behavior. Histamine might also play an important role in compound 48/80-induced scratching behavior.     

Pentacyclic triterpenoids, alpha,beta-amyrins, suppress the scratching behavior in a mouse model of pruritus

In the search for natural compounds useful against pruritus, alpha,beta-amyrins, the pentacyclic triterpenes isolated from the resin of popular medicinal plant Protium heptaphyllum were examined on scratching behavior induced by dextran T40 and compound 48/80 in mice. The animals were pretreated orally with alpha,beta-amyrins (50, 100 and 200 mg/kg) or cyproheptadine (10 mg/kg), an antagonist of histamine and serotonin receptors and 2 h later, they were given subcutaneous injections of dextran T40 (75 mg/kg) or compound 48/80 (3 mg/kg) into the rostral back, and scratching was quantified for 20 min. The scratching behavior induced by dextran T40 and compound 48/80 was significantly inhibited in mice pretreated with alpha,beta-amyrins (100 and 200 mg/kg) or cyproheptadine (10 mg/kg), In addition, the compound 48/80-elicited degranulation of rat peritoneal mast cells (ex vivo) was also markedly reduced in animals pretreated with alpha,beta-amyrins (100 mg/kg) or ketotifen (1 mg/kg), a known mast cell stabilizer. In the open-field test, alpha,beta-amyrins (100 and 200 mg/kg)-pretreated mice showed no impairment of spontaneous locomotion, suggesting that these triterpenoids possess no sedative activity that could account for suppression of scratching behavior. These results clearly indicate the antipruritic effect of alpha,beta-amyrins and suggest that this effect may be related to a stabilizing action on mast cell membrane.     

Inhibitory effects of Moutan cortex on immediate allergic reactions

The anti-allergic effect of an ethanol extract from Moutan Cortex was evaluated in some animal models. The Moutan Cortex extract (30, 100 mg/kg, i.p.) dose-dependently inhibited systemic anaphylactic shock induced by compound 48/80 in mice. It also inhibited dose-dependently the scratching behavior induced by compound 48/80 or histamine at a dose of 100 mg/kg. An increase in the vascular permeability induced by compound 48/80 or histamine was also inhibited by the Moutan Cortex. In addition, in vitro studies, the Moutan Cortex inhibited histamine release from rat peritoneal mast cells induced by compound 48/80. To investigate the active component of Moutan Cortex extract, it was suspended in water and extracted with EtOAc to yield EtOAc insoluble (A) and soluble (B) fractions. The effect of extract (B) was more potent than that of extract (A) in inhibiting histamine release. From these findings, it seems likely that the Moutan Cortex extract is effective in antagonizing certain pharmacological effects induced by compound 48/80, which is probably mediated by inhibiting the release of histamine from mast cells and antagonizing the effect on histamine. The main active component of Moutan Cortex is considered to be contained in extract (B). In conclusion, Moutan Cortex may be useful for the relief of symptoms of atopic dermatitis and other allergy-related diseases.     

Potent pruritogenic action of tryptase mediated by PAR-2 receptor and its involvement in anti-pruritic effect of nafamostat mesilate in mice

The pruritogenic potency of tryptase and its involvement in anti-pruritic effect of intravenous nafamostat mesilate (NFM) were studied in mice. An intradermal injection of tryptase (0.05-1 ng/site) elicited scratching in ICR mice, while chymase was without effects at doses of 0.05-50 ng/site. The dose-response curve of tryptase action was bell-shaped and the effect peaked at 0.1 ng/site (approximately 0.7 fmol/site). NFM (10 mg/kg) inhibited scratching induced by tryptase but not by histamine and serotonin. NFM (1-10 mg/kg) produced the dose-dependent inhibition of scratching induced by intradermal compound 48/80 (10 microg/site). The inhibition by NFM (10 mg/kg) was abolished in mast cell-deficient (WBB6F1 W/W(V)) mice, but not in wild-type (WBB6F1 +/+) mice. NFM (10 mg/kg) suppressed tryptase activity in the mouse skin. Proteinase-activated receptor-2 (PAR-2) neutralizing antibody (0.1 and 1 microg/site) and the PAR-2 antagonist FSLLRY (10 and 100 microg/site) inhibited scratching induced by tryptase (0.1 ng/site) and compound 48/80 (10 microg/site). These results suggest that mast cell tryptase elicits itch through PAR-2 receptor and that NFM inhibits itch-associated responses mainly through the inhibition of mast cell tryptase.     

Antipruritic effect of ginsenoside rb1 and compound k in scratching behavior mouse models

The antipruritic and vascular permeability-inhibitory effects of ginsenoside Rb1, a main component of ginseng frequently used as a traditional medicine in Asian countries, and its metabolite compound K by intestinal microflora were investigated in scratching behavior animal models induced by compound 48/80, substance P, and histamine. Ginsenoside Rb1 and compound K orally administered 1 and 6 h before the treatment of compound 48/80 showed antipruritic effect. These ginsenosides administered at a dose of 50 mg/kg 6 h before the treatment of compound 48/80 inhibited scratching behaviors by 51% and 64%, respectively, compared with that of the control. These ginsenosides also inhibited the vascular permeability of skin. Compound K intraperitoneally administered 1 h before the treatment of compound 48/80 potently inhibited the scratching behaviors induced by compound 48/80. However, intraperitoneally administered ginsenoside Rb1 did not inhibit scratching behaviors. Compound K inhibited compound 48/80-, substance P-, and histamine-induced scratching behaviors, with 50% inhibitory doses of 4.2, 5.9, and 3.8 mg/kg, respectively, and vascular permeability, with 50% inhibitory doses of 5.8, 6.8, and 4.1 mg/kg, respectively. These results suggest that ginsenoside Rb1 and its metabolite compound K by intestinal microflora can improve scratching behaviors.     

Effect of Usuhiratake (Pleurotus pulmonarius) on sneezing and nasal rubbing in BALB/c mice

The anti-rhinitis properties of Pleurotus pulmonarius were investigated in BALB/c mice. A single administration of Pleurotus Pulmonarius caused no significant effect on antigen-induced nasal rubbing and sneezing at a dose of 500 mg/kg, but a significant inhibition was observed after 2 weeks of repeated treatment at this dose, and at a dose of 200 mg/kg, it also caused a significant inhibition after repeated administration for 4 weeks. Pleurotus pulmonarius showed no significant inhibitory effect on the production of IgE. In addition, Pleurotus pulmonarius caused no inhibition of histamine-induced nasal rubbing and sneezing at a dose of 500 mg/kg, but in vitro study, it inhibited histamine release from rat mast cells induced by compound 48/80 at the soluble supernatant solution of 30 and 100 microg/ml of Pleurotus pulmonarius suspended in PBS. These results demonstrated that Pleurotus pulmonarius may be effective in the relief of symptoms of allergic rhinitis through inhibition of histamine release.     

Antiallergic and anti-inflammatory properties of the ethanolic extract from Gleditsia sinensis

This study was carried out to determine the effects of the 70% ethanolic extract from the anomalous fruits of Gleditsia sinensis LAM. (AFGS) on experimental allergic reactions and inflammation. AFGS (200, 500, 1000 mg/kg, p.o.) dose-dependently inhibited the systemic anaphylactic shock induced by compound 48/80 in mice and cutaneous reactions induced by histamine or serotonin in rats. At doses of 500 and 1000 mg/kg, AFGS showed a clear inhibition on homologous passive cutaneous anaphylaxis in rats. In vitro, AFGS significantly reduced histamine release from rat peritoneal mast cells triggered by compound 48/80 at concentrations of 20 and 50 micro/ml. Moreover, AFGS (500, 1000 mg/kg, p.o.) showed a significant inhibition on the hind paw edema in rats and ear swelling in mice caused by carrageenin and croton oil, respectively. It also clearly inhibited the vascular permeability induced by acetic acid in mice at a dose of 1000 mg/kg. These findings demonstrate that the ethanolic extract from the anomalous fruits of Gleditsia sinensis possesses antiallergic and anti-inflammatory activities, which may be mediated by reducing the release of mediators such as histamine from mast cells and weakening the inflammatory action of these mediators.     

Antiallergic effects of astemizole on immediate type hypersensitivity reactions.

Astemizole (0.5-5 mg/kg, p.o.) dose-dependently inhibited heterologous and homologous PCA reactions in rats at ID50 values of 1.48 mg/kg and 2.37 mg/kg, respectively. The inhibitory effect of astemizole on heterologous PCA was most remarkable when this compound was given p.o. 2 h prior to antigen challenge. Astemizole (0.1-5 mg/kg, p.o.) dose-dependently inhibited experimentally-induced asthma in guinea pigs at an ID50 of 0.86 mg/kg. Ex vivo, astemizole (0.5-5 mg/kg, p.o.) inhibited antigen-induced histamine release from lung pieces of sensitized guinea pigs. In in vitro experiments, the drug dose-dependently inhibited antigen-induced histamine and SRS-A releases from guinea pig lung pieces at concentrations of 0.05-10 microM. Furthermore, astemizole (0.1-10 microM) inhibited the histamine release induced by compound 48/80 and antigen-antibody reaction from rat peritoneal mast cells, and at 0.1-500 nM inhibited both leukotriene C4- and platelet-activating factor (PAF)-induced contraction of isolated guinea pig trachea at submicromolar concentrations. Astemizole not only inhibited 45Ca uptake into rat mast cells but also prevented the Ca2+ release from the intracellular Ca store induced by compound 48/80, although this compound did not affect the histamine release from permeabilized mast cells induced by Ca2+. Our results suggest that one of the antiallergic mechanisms of astemizole may be an inhibition of signal transduction from the mast cell membrane to the intracellular systems.     

Topical application of luteolin inhibits scratching behavior associated with allergic cutaneous reaction in mice

The present study is aimed at evaluating the effects of luteolin on the scratching behavior associated with an allergic cutaneous reaction in mice. Elicitation of passive cutaneous anaphylaxis, and intradermal injections of compound 48/80, histamine or serotonin induced scratching behavior in ICR mice. Models of irritant contact dermatitis and allergic contact dermatitis were prepared by the topical application of 2,4-dinitrochlorobenzene (DNCB) on the ears of mice. Topical application of luteolin at concentrations of 20 and 100 mug/site significantly inhibited the number of scratching incidents associated with passive cutaneous anaphylaxis, and a similar tendency was also observed in histamine-, serotonin- and compound 48/80-evoked cutaneous reactions. The vascular permeability increase induced by passive cutaneous anaphylaxis or histamine injection was also significantly reduced by luteolin. Luteolin showed a potent inhibition on the ear thickness increase in models of irritant contact dermatitis and allergic contact dermatitis. In conclusion, luteolin significantly inhibited the scratching behavior associated with allergic cutaneous anaphylaxis. Its effects against pruritus are mainly attributed to its inhibition of mediator release from activated mast cells and direct antagonist effects on the released mediators which may act as local pruritogens.     

Involvement of unique mechanisms in the induction of scratching behavior in BALB/c mice by compound 48/80

Compound 48/80 induced scratching behavior in BALB/c mice, and the role of mast cell mediators in this behavior was examined. Mouse scratching behavior was detected and evaluated using a new apparatus, MicroAct. Compound 48/80 increased the incidence of scratching behavior and scratching time in a dose-dependent manner, accompanied by a potent activation of mast cells and a potent increase in vascular permeability. Dibucaine and mu-opioid receptor antagonists inhibited the scratching behavior. Although histamine H(1) receptor antagonists potently inhibited the vascular permeability increase, they did not affect the scratching behavior. Methysergide inhibited the scratching behavior slightly without affecting the vascular permeability increase, whereas cyproheptadine inhibited both. A cyclooxygenase inhibitor, a 5-lipoxygenase-activating protein inhibitor and a PAF receptor antagonist did not affect the scratching behavior. High doses of serotonin induced scratching behavior less frequently than did compound 48/80. Furthermore, mast cell-deficient WBB6F1-W/W(v) mice exhibited frequent scratching behavior after injection of compound 48/80. These results clearly indicate that compound 48/80 can induce scratching behavior in mice independent of mast cell mediators.     

Inhibition of immediate allergic reactions by ethanol extract from Plumbago zeylanica stems

The antiallergic properties of the 70% ethanol extract from Plumbago zeylanica stems (EPZ) were investigated in the present study. The extract (500, 1000 mg/kg, p.o.) dose-dependently inhibited systemic anaphylactic shock induced by compound 48/80 in mice, reduced homologous passive cutaneous anaphylaxis and skin reactions induced by histamine or serotonin in rats, significant differences were observed at the dose of 1000 mg/kg. In vitro, EPZ (5, 20, 50 microg/ml) concentration-dependently reduced histamine release from rat peritoneal mast cells caused by compound 48/80 and antigen. EPZ (50 microg/ml) markedly increased intracellular cAMP content of rat mast cells. These findings demonstrate that EPZ inhibits mast cell-dependent immediate allergic reactions, which is probably mediated by reducing the release of mediators such as histamine from mast cells via elevating intracellular cAMP level and weakening the inflammatory action of mediators.     

Inhibitory effect of mast cell-mediated immediate-type allergic reactions by Cichorium intybus.

We investigated the effect of an aqueous extract of Cichorium intybus (CIAE) on mast cell-mediated immediate type allergic reactions. CIAE (0.1-1000 mg kg-1) dose-dependently inhibited systemic anaphylactic reaction induced by compound 48/80 in mice. Especially, CIAE inhibited compound 48/80-induced anaphylactic reaction 100% with the dose of 1000 mg kg-1. CIAE 1000 mg kg-1also significantly inhibited local anaphylactic reaction activated by anti-dinitrophenyl (DNP) IgE. When mice were pretreated with CIAE at a concentration ranging from 0.1 to 1000 mg kg-1, the plasma histamine levels were reduced in a dose-dependent manner. CIAE (1-1000 microg ml-1) dose-dependently inhibited histamine release from the rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cAMP in RPMC, when CIAE (1000 microg ml-1) was added, increased significantly compared with that of control cells. These results indicate that CIAE inhibits mast cell-mediated immediate-type allergic reactions in vivo and in vitro.     

Possible role of mast cells in cineole-induced scratching behavior in mice.

We examined the scratch (itch) inducing effect of 1,8-cineole (cineole), a monoterpene oxide present in many plant essential oils and the possible role of mast cells in the response. Subcutaneous injection of cineole (10, 20 and 40 microl/site) or the mast cell degranulating agent, compound 48/80 (25, 50 and 100 microg/site) into the rostral back of mice induced a scratching behavior. This response of cineole as well as that of 48/80 was markedly suppressed in mice subjected to mast cell desensitization by repeated injections of 48/80. The cineole-induced scratching was also significantly diminished in animals pretreated with diphenhydramine, the histamine H1-receptor antagonist or cyproheptadine, the dual histamine/serotonin-receptor antagonist. Furthermore, the scratch-inducing effect of cineole was greatly reduced in mice that received the opioid antagonist naloxone or the selective adenosine A1-receptor agonist, N6-cyclopentyladenosine (CPA), but not the more selective adenosine A2-receptor agonist, 5'-N-ethylcarboxamidoadenosine (NECA). The data suggest a likely role for mast cells in cineole-induced scratching behavior of mice, possibly involving adenosinergic and opioidergic mechanisms.     

Magnoliae flos inhibits mast cell-dependent immediate-type allergic reactions.

The mast cell plays a pivotal role in initiating allergic response by secreting intracytoplasmic granular mediators such as histamine. Magnoliae flos has been used for the treatment of allergic disease in Korea. However, its effect in experimental models remains unknown. The present report describes an inhibitory effect of Magnoliae flos on mast cell-mediated immediate-type allergic reactions. Topical application of compound 48/80 can induce an ear swelling response in normal (WBB6F1-+/+) mice but not in the congenic mast cell-deficient WBB6F1-W/Wv mice. Magnoliae flos inhibited concentration-dependently mast cell-dependent ear swelling response induced by compound 48/80 by topical application. Magnoliae flos inhibited concentration-dependently passive cutaneous anaphylaxis induced by anti-dinitrophenyl (DNP) IgE in rats by topical application. Magnoliae flos also inhibited concentration-dependently the histamine release from the rat peritoneal mast cells by compound 48/80 or anti-DNP IgE. Moreover, Magnoliae flos had a significant inhibitory effect on compound 48/80-induced systemic anaphylactic reaction. These results indicate that Magnoliae flos inhibits immediate-type allergic reactions by inhibition of mast cell degranulation in vivo and in vitro.     

Physiological activities of S-(1,2-dicarboxyethyl)glutathione as an intrinsic tripeptide present in liver, heart and lens.

S-(1,2-Dicarboxyethyl)glutathione (DCE-GS, CAS 1115-52-2) found in rat liver, heart and lens in considerable amounts, showed an anti-inflammatory effect, which was evaluated by testing the inhibition of the experimental conjunctival edema of rats. An intravenous injection (3 mg/kg) prior to the carrageenan injection prevented the conjunctive edema formation by up to 30%. This peptide also inhibited the histamine release from rat mast cells induced by the compound 48/80. The peptide was added to the mast cells before addition of the compound 48/80 and an inhibition of the histamine release up to 96% at a 1 mmol/l concentration occurred. Furthermore, it displayed an antianaphylactic effect in rats using antibody against chicken egg albumin. An injection of the peptide (30 mg/kg) prior to the antigen administration inhibited color deposition up to 43%. Analogues or derivatives of DCE-GS were synthesized and tested for those inhibitory activities. However, there was no other peptide having stronger effects than DCE-GS and little structure-activity relationship among them.     

The protective effect of Tinospora cordifolia on various mast cell mediated allergic reactions

This study investigated the effect of an aqueous extract of Tinospora cordifolia (Willd.) Miers (Menispermaceae) stem on mast cell mediated allergic reactions in vivo and in vitro and studied its possible mechanism. T. cordifolia (125 to 1000?mg/kg) dose-dependently inhibited compound 48/80 induced lethality in rats, histamine induced paw edema in mice and histamine induced bronchial asthma in guinea pigs. T. cordifolia significantly (p?<?0.001) inhibited the cutaneous anaphylaxis reaction activated by histamine in a rat model and compound 48/80 induced ear swelling response in mice. T. cordifolia (2.5-160?μg/mL) also showed significant (p?<?0.001) inhibition of histamine induced contraction of guinea-pig ileum in vitro implying the H₁ antihistamine activity. T. cordifolia (0.01 to 10?mg/mL) significantly (p?<?0.001) inhibited the histamine release from rat peritoneal mast cells activated by compound 48/80. In addition, T. cordifolia (0.01 to 10?mg/mL) significantly (p?<?0.001) inhibited the secretion of tumor necrosis factor-α (TNF-α) in antidinitrophenyl (DNP) IgE-stimulated rat peritoneal mast cells. The level of cAMP in RPMC transiently and significantly increased compared with that of control cells when T. cordifolia was incubated with mast cells. T. cordifolia (0.01 to 10?mg/mL) showed concentration-dependent inhibition in compound 48/80 induced reactive oxygen species (ROS) generation. In addition, T. cordifolia decreased intracellular calcium levels of activated mast cells. These results show that T. cordifolia may be beneficial in the treatment of acute and chronic allergic disorders.