Participation in cysteinyl leukotrienes and thromboxaneA2 in nasal congestion model in Brown Norway rats

Kishi, Yuko; Nakano, Yoshitaka; Jiang, Shuishi; Yatsuzuka, Rie; Kamei, Chiaki

doi:10.1016/j.intimp.2007.05.020

Cited by 8 publications

(6 citation statements)

References 29 publications

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“…Almost the identical findings were already reported by ours. 8,9) In other words, an increase in Penh observed after TDI challenge was reconfirmed even in the present study. It was found that 17-phenyl trinor PGE 2 and butaprost had no significant effect on an increase of Penh in early phase after TDI challenge in sensitized rats.…”

Section: Discussionsupporting

confidence: 83%

“…8) In this model, the animals showed not only sneezing but also nasal congestion in the early and late phases.…”

mentioning

confidence: 93%

“…[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.…”

mentioning

confidence: 99%

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Participation of Prostaglandin E2 Receptor in Nasal Congestion of Brown Norway Rats

Kurata

Yamamoto

Izawa

et al. 2010

Biological & Pharmaceutical Bulletin

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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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Section: Discussionsupporting

confidence: 83%

“…8) In this model, the animals showed not only sneezing but also nasal congestion in the early and late phases.…”

mentioning

confidence: 93%

mentioning

confidence: 99%

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Participation of Prostaglandin E2 Receptor in Nasal Congestion of Brown Norway Rats

Kurata

Yamamoto

Izawa

et al. 2010

Biological & Pharmaceutical Bulletin

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“…Like leukotrienes, thromboxanes are arachidonic acid derivatives, released from mast cells and other inflammatory cells, that are found in nasal lavage fluid samples following nasal allergen challenge 24,25. In animal models, TXA2 agonists increase nasal airway resistance and vascular permeability.…”

Section: Mucosal Inflammationmentioning

confidence: 99%

Pathophysiology of nasal congestion

Naclerio¹

2010

IJGM

105

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Nasal congestion is a common symptom in rhinitis (both allergic and nonallergic), rhinosinusitis and nasal polyposis. Congestion can also be caused by physical obstruction of nasal passages and/or modulation of sensory perception. Mucosal inflammation underlies many of the specific and interrelated factors that contribute to nasal congestion, as well as other symptoms of both allergic rhinitis and rhinosinusitis. A wide range of biologically active agents (eg, histamine, tumor necrosis factor-α, interleukins, cell adhesion molecules) and cell types contribute to inflammation, which can manifest as venous engorgement, increased nasal secretions and tissue swelling/edema, ultimately leading to impaired airflow and the sensation of nasal congestion. Inflammation-induced changes in the properties of sensory afferents (eg, expression of peptides and receptors) that innervate the nose can also contribute to altered sensory perception, which may result in a subjective feeling of congestion. Increased understanding of the mechanisms underlying inflammation can facilitate improved treatment selection and the development of new therapies for congestion.

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“…It has been reported that seratrodast showed an inhibitory effect on the increase of nasal congestion, but did not suppress the sneezing frequency in the allergic rhinitis model. [15][16][17] On the other hand, Yamasaki et al reported that the intranasal application of U-46619, a TXA 2 receptor agonist, caused no sneezing in guinea pigs. 18) This finding is consistent with our result in the present study.…”

Section: Discussionmentioning

confidence: 99%

Prophylactic Effects of the Histamine H1 Receptor Antagonist Epinastine and the Dual Thromboxane A2 Receptor and Chemoattractant Receptor-Homologous Molecule Expressed on Th2 Cells Antagonist Ramatroban on Allergic Rhinitis Model in Mice

Suzuki

Inoue

Yamamoto

et al. 2011

Biological & Pharmaceutical Bulletin

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Participation in cysteinyl leukotrienes and thromboxaneA2 in nasal congestion model in Brown Norway rats

Cited by 8 publications

References 29 publications

Participation of Prostaglandin E2 Receptor in Nasal Congestion of Brown Norway Rats

Participation of Prostaglandin E2 Receptor in Nasal Congestion of Brown Norway Rats

Pathophysiology of nasal congestion

Prophylactic Effects of the Histamine H1 Receptor Antagonist Epinastine and the Dual Thromboxane A2 Receptor and Chemoattractant Receptor-Homologous Molecule Expressed on Th2 Cells Antagonist Ramatroban on Allergic Rhinitis Model in Mice

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