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We studied the effect of Brazilian propolis on sneezing and nasal rubbing in experimental allergic rhinitis of mice. A single administration of propolis caused no significant effect on both antigen-induced nasal rubbing and sneezing at a dose of 1000 mg/kg, but a significant inhibition was observed after repeated administration for 2 weeks at this dose. Propolis caused no significant inhibitory effect on the production of total IgE level after repeated administration of 1000 mg/kg. The drug also caused no significant inhibition of histamine-induced nasal rubbing and sneezing at a dose of 1000 mg/kg. On the other hand, propolis significantly inhibited histamine release from rat mast cells induced by antigen and compound 48/80 at a concentration of more than 10 microg/ml. These results clearly demonstrated that propolis may be effective in the relief of symptoms of allergic rhinitis through inhibition of histamine release.

We investigated the synergetic effects of glucocorticoid and histamine H1 receptor antagonists on an atopic dermatitis model. Hairless mice were used in this study and an atopic dermatitis model was made by repeated application of 2,4,6-trinitrochlorobenzene. The effects of glucocorticoid, histamine H1 receptor antagonists, and the simultaneous use of these drugs were investigated by measuring scratching behavior, skin symptoms and nerve growth factor (NGF) in the skin. Topical application of prednisolone significantly inhibited scratching behavior, skin symptoms and NGF contents in the skin by repeated application. Olopatadine also showed a significant effect on scratching behavior and NGF contents in the skin, whereas chlorpheniramine showed no significant inhibitory effect on these indices. Furthermore, the combined use of prednisolone and olopatadine potentiated the inhibition of scratching behavior, skin symptoms, and NGF in the skin. From these findings, olopatadine potentiated the inhibitory effect of prednisolone on the symptoms of atopic dermatitis by inhibiting NGF.

It is well known that histamine, cysteinyl leukotriene (cysLTs), thromboxanes, prostaglandins (PGs) and cytokines are responsible for allergic rhinitis. 1,2) There are two phases of allergic rhinitis response, named "early phase" and "late phase." Early phase response occurs within minutes of exposure to the allergen and is characterized by sneezing, rhinorrhea and nasal congestion. Late phase response occurs 4 to 8 h after allergen exposure and is characterized mainly by nasal congestion. 3)Histamine H 1 receptor antagonists, such as chlorpheniramine and astemizol, are widely used to treat allergic rhinitis clinically, 4,5) however, these H 1 receptor antagonists are not completely effective for nasal congestion. [6][7][8] In an animal model, we have reported that although H 1 receptor antagonists inhibited the increase of enhanced pause (Penh) in early phase induced by toluene 2,4-diisocyanate (TDI) challenge, 9) a relatively high dose was needed. On the other hand, we reported that cys-LTs receptor antagonists (pranlukast, zafirlukast) and thromboxane A 2 (TXA 2 ) receptor antagonists (seratrodast, ramatroban) also caused an inhibitory effect on the increase of Penh in early and late phases after TDI challenge in sensitized rats. 10) Therefore, it seems likely that different mediator is involved in early and late phase responses in nasal congestion.Prostaglandin E 2 (PGE 2 ) is arachidonic acid metabolite similar to LTs and TXA 2 , and there are four different receptors designated EP 1 , EP 2 , EP 3 and EP 4 . Kunikata et al. 10) reported that mice lacking EP 3 receptor developed potent allergic inflammation compared with wild-type mice or mice deficient in other prostaglandin E 2 receptor subtypes. On the other hand, Gomi et al.11) described that PGE 2 selectively enhanced the immunoglobulin E (IgE)-mediated production of interleukin-6 (IL-6). These actions may produce by the receptors other than EP 3 receptor.In a previous study, we established a nasal congestion model using Brown Norway (BN) rats by intranasal immunization with toluene 2,4-diisocyanate (TDI) as an antigen. 8)In this model, the animals showed not only sneezing but also nasal congestion in the early and late phases.In the present study, in order to clarify the role of PGE 2 receptor (EP 1 , EP 2 , EP 3 and EP 4 ) in the development of allergic rhinitis symptoms, we investigated the effects of each PGE 2 receptor agonists with a nasal congestion model in BN rats. MATERIALS AND METHODSAnimals Six-week-old male BN rats were obtained from Kyudo Co., Ltd. (Saga, Japan). The animals were housed in an air-conditioned room, maintained at 24Ϯ2°C, with relative humidity of 55Ϯ10%. The rats were given standard laboratory rodent food (Oriental Yeast, Tokyo, Japan) and water ad libitum. All procedures involving animals were conducted in accordance with the Guidelines for Animal Experiments at Okayama University Advanced Science Research Center.Materials The following reagents were obtained from the sources shown in parentheses: TDI (Wako, Tokyo, Japan)...

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