Evidence for the contribution of tumour necrosis factor in oedema formation induced by histamine in the hind paw of the rat

被引：7

作者：

Kalokasidis, K. ^{[1
]}

Molyva, D. ^{[1
]}

Mirtsou, V. ^{[1
]}

Kokkas, B. ^{[1
]}

Goulas, A. ^{[1
]}

机构：

[1] Aristotle Univ Thessaloniki, Sch Med, Dept Pharmacol 1, Thessaloniki 54124, Greece

来源：

INFLAMMATION RESEARCH | 2009年 / 58卷 / 08期

关键词：

Histamine; Tumour necrosis factor; Oedema; Rat paw; TNF-ALPHA RELEASE; MAST-CELLS; RECEPTORS; KINASE; H-1-ANTIHISTAMINES; THALIDOMIDE; MECHANISMS; EXPRESSION; LINE;

D O I：

10.1007/s00011-009-0047-1

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

There is mounting evidence that tumour necrosis factor (TNF) is involved in the early phase of inflammatory response, but its relation to histamine action is unclear. In this study we examined the effect of drugs interfering with TNF expression (thalidomide) and activity (infliximab) and compared it to that of a H1R histamine receptor antagonist (loratadine) in a model of histamine-induced rat hind-paw oedema formation. Systemic administration of all three drugs effectively reduced the oedema formed by the subsequent transplantar administration of histamine into the rat paw, in a dose-dependent manner. The time-dependence of the effect exerted by thalidomide and infliximab was very similar to that of loratadine. Moreover, there appears no significant synergistic effect between infliximab and loratadine, suggesting that TNF is either a major modulator or a direct mediator of oedema formation induced by histamine, in the rat paw.

引用

页码：437 / 440

页数：4

共 20 条

[1] Protein kinase C-α a mediates TNF release process in RBL-2H3 mast cells [J].

Abdel-Raheem, IT ;

Hide, I ;

Yanase, Y ;

Shigemoto-Mogami, YS ;

Sakai, N ;

Shirai, Y ;

Saito, N ;

Hamada, FM ;

El-Mahdy, NA ;

Sakai, N ;

Shirai, Y ;

Saito, N ;

Hamada, FMH ;

El-Mahdy, NA ;

Elsisy, AEDE ;

Sokar, SS ;

Nakata, Y .

BRITISH JOURNAL OF PHARMACOLOGY, 2005, 145 (04) :415-423

[2] Histamine receptors are hot in immunopharmacology [J].

Akdis, CA ;

Simons, FER .

EUROPEAN JOURNAL OF PHARMACOLOGY, 2006, 533 (1-3) :69-76

[3] Activation of endothelial nitric-oxide synthase by tumor necrosis factor-α:: A novel pathway involving sequential activation of neutral sphingomyelinase, phosphatidylinositol-3′ kinase, and Akt [J].

Barsacchi, R ;

Perrotta, C ;

Bulotta, S ;

Moncada, S ;

Borgese, N ;

Clementi, E .

MOLECULAR PHARMACOLOGY, 2003, 63 (04) :886-895

[4] Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B1 receptors in the rat paw [J].

Fernandes, ES ;

Passos, GF ;

Campos, MM ;

Araújo, JGVC ;

Pesquero, JL ;

Avelllar, MC ;

Teixeira, MM ;

Calixto, JB .

BRITISH JOURNAL OF PHARMACOLOGY, 2003, 139 (05) :973-981

[5]

Hide I, 1997, J IMMUNOL, V159, P2932

[6] Regulation of endothelial permeability by Src kinase signaling: Vascular leakage versus transcellular transport of drugs and macromolecules [J].

Hu, Guochang ;

Place, Aaron T. ;

Minshall, Richard D. .

CHEMICO-BIOLOGICAL INTERACTIONS, 2008, 171 (02) :177-189

[7] Bidirectional communication between histamine and cytokines [J].

Igaz, P ;

Novák, I ;

Lázár, E ;

Horváth, B ;

Héninger, E ;

Falus, A .

INFLAMMATION RESEARCH, 2001, 50 (03) :123-128

[8] H1-antihistamines:: inverse agonism, anti-inflammatory actions and cardiac effects [J].

Leurs, R ;

Church, MK ;

Taglialatela, M .

CLINICAL AND EXPERIMENTAL ALLERGY, 2002, 32 (04) :489-498

[9]

Marone Gianni, 2003, Journal of Allergy and Clinical Immunology, V112, pS83, DOI 10.1016/S0091-6749(03)01881-5

[10] THALIDOMIDE EXERTS ITS INHIBITORY-ACTION ON TUMOR-NECROSIS-FACTOR-ALPHA BY ENHANCING MESSENGER-RNA DEGRADATION [J].

MOREIRA, AL ;

SAMPAIO, EP ;

ZMUIDZINAS, A ;

FRINDT, P ;

SMITH, KA ;

KAPLAN, G .

JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 177 (06) :1675-1680

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