A bradykinin (BK)<sub>1</sub> receptor antagonist blocks capsaicin‐induced ear inflammation in mice

Mantione, Charles R.; Rodríguez, Richard

doi:10.1111/j.1476-5381.1990.tb12960.x

Cited by 50 publications

(28 citation statements)

References 10 publications

(11 reference statements)

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“…Then oedema gradually decreased with time but erythema was attenuated at 2 h. A dose-dependent enhancement of oedema development was not observed with increased concentrations of capsaicin (100-1000 ftg). In the subsequent experiments, induction of ear oedema was performed by treatment with capsaicin at a dose of 250 ytg, which is the same dose as previously studied (Mantione & Rodriguez, 1990). …”

Section: Resultsmentioning

confidence: 99%

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Profile of capsaicin‐induced mouse ear oedema as neurogenic inflammatory model: comparison with arachidonic acid‐induced ear oedema

Inoue

Nagata

Kinoshita

1993

British J Pharmacology

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1 We have investigated the mechanism of capsaicin-induced mouse ear oedema compared with that of arachidonic acid (AA)-induced ear oedema, and evaluated the possible involvement of neuropeptides in the development of capsaicin-induced oedema. 2 Topical application of capsaicin (0.1-1.0 mg per ear) to the ear of mice produced immediate vasodilatation and erythema followed by the development of oedema which was maximal at 30 min after the treatment. This oedema was of shorter duration with less swelling than AA-induced oedema (2.0 mg per ear). 3 Capsaicin-induced ear oedema was unaffected when inhibitors of arachidonate metabolites including platelet activating factor (PAF) were administered before capsaicin (250 jg per ear) application, while these agents significantly prevented AA-induced oedema. Dexamethasone, histamine HI and/or 5-hydroxytryptamine (5-HT) antagonists, and substance P (SP) antagonists were effective in inhibiting both models. Furthermore, a Ca2+-channel blocker and the capsaicin inhibitor, ruthenium red, were effective inhibitors of capsaicin oedema but had no effect on AA-induced oedema.4 Phosphoramidon (50 jig kg-', i.v.), an endopeptidase inhibitor, markedly (P<0.001) enhanced only capsaicin-induced ear oedeima, but bestatin (0.5mgkg-', i.v.), an aminopeptidase, failed to enhance oedema formation. 5 Neuropeptides (1-100 pmol per site) such as rat calcitonin gene-related peptide (CGRP), SP, neurokinin A (NKA), and vasoactive intestinal peptide (VIP), which are released from capsaicinsensitive neurones, caused ear oedema by intradermal injection. Furthermore, a synergistic effect of CGRP (10fmol per site) and SP (1Opmol per site) on oedema formation was observed.6 The oedema induced by neuropeptides was significantly (P<0.05 or P<0.001) inhibited when cyproheptadine (20 mg kg-', p.o.), a histamine H, and 5-HT antagonist, was administered before injection. In contrast, nifedipine (50 mg kg-', p.o.), a Ca2'-channel blocker, and indomethacin (10 mg kg-', p.o., except for NKA), a cyclo-oxygenase inhibitor, had little effect on neuropeptideinduced oedema. 7 These results suggest that the mechanism of capsaicin-induced ear oedema is different from that of AA-induced oedema and suggest that the development of capsaicin-induced ear oedema is primarily mediated by neuropeptides. The neuropeptides released after activation of sensory nerves cause an increase of vascular permeability by interactions with endothelial cells and by histamine release from mast cells.

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Section: Resultsmentioning

confidence: 99%

“…Recently, it has been reported that capsaicin can induce acute inflammation in the mouse ear (Mantione & Rodriguez, 1990;Gabor & R'azga, 1992) and rat paw (De & Ghosh, 1990). However, direct evidence for the participation of mediators in this inflammatory response is lacking.…”

Section: Introductionmentioning

confidence: 99%

Profile of capsaicin‐induced mouse ear oedema as neurogenic inflammatory model: comparison with arachidonic acid‐induced ear oedema

Inoue

Nagata

Kinoshita

1993

British J Pharmacology

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“…[28][29][30] Also, plants and plant-originated substances have relevance in dermatology for both their adverse and beneficial effects on skin disorders and the skin in general. 31) Amongst the plant-derived natural products, the most effective groups with the inhibitory properties against contact dermatitis are the phenolics and terpenoids.…”

Section: Discussionmentioning

confidence: 99%

Topically Applied Diterpenoids from Egletes viscosa (Asteraceae) Attenuate the Dermal Inflammation in Mouse Ear Induced by Tetradecanoylphorbol 13-Acetate- and Oxazolone

Calou

Sousa

Andrade

et al. 2008

Biological & Pharmaceutical Bulletin

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Over the past three decades, the prevalence of atopic dermatitis and allergic or irritant contact dermatitis has been increasing significantly in the general population, causing considerable economic costs and decreased quality of life. [1][2][3] Topical corticosteroids have been the first-choice therapy for treatment of these inflammatory skin diseases such as eczema, atopic and seborrheic dermatitis, and psoriasis. While effective in many patients, this form of therapy carry the concern of local and systemic adverse effects and may induce skin atrophy, especially after long-term use. 4,5) In contrast to topical corticosteroids, the more recently introduced calcineurin inhibitors like tacrolimus and pimecrolimus do not induce skin atrophy, even after long-term use but may induce adverse effects such as burning, erythema and pruritus and are contraindicated in patients younger than two years or in those who are immunosuppressed.6,7) Thus, the available drugs, although have efficacy they are associated with adverse effects and therefore the development of new and safe anti-inflammatory topical agents for the treatment of dermatitis is needed.Studies reveal that a large percentage of patients use some form of complementary and alternative medicine for the treatment of atopic and contact dermatitis, which include herbal remedies. [8][9][10] In the recent past, several diterpene compounds of plant origin such as abietic acid from Pimenta racemosa var. grissea, hypoestoxide from Hypoestes rosea and marrubiin from Marrubium vulgare were shown to be effective in the mouse model of ear edema induced by several phlogestogens like histamine, bradykinin, capsaicin, prostaglandin E 2 , Croton oil, TPA (12-O-tetradecanoylphorbol 13-acetate) or oxazolone.11-13) Centipedic acid (CA) and 12-acetoxy-hawtriwaic acid lactone (AHAL, Tanabalin) are the naturally occurring diterpenes isolated from the aerial parts of Egletes viscosa L. (Asteraceae), a traditional medicinal plant.14) Previously we reported on the gastroprotective and antinociceptive properties of these diterpenes as well as an anti-edematogenic activity of tanabolin against ear edema induced by capsaicin. 15,16) However, the anti-inflammatory efficacy of these two diterpene compounds was not tested in the models of ear edema induced by either TPA or oxazolone, the most commonly used ones for analysing the agents effective against contact or atopic dermatitis.17,18) Thus as a part of our continuation study, we describe here for the first time the anti-dermatitis effects of these two natural diterpenes from Egletes viscosa using the experimental models of acute and chronic dermatitis induced by TPA and oxazolone, respectively, in the mouse ear. MATERIALS AND METHODS Plant Material and Isolation of DiterpenoidsThe aerial parts (2.5 kg) of Egletes viscosa LESS. (Asteraceae) were collected from the experimental plantation pertaining to the Department of Agronomy of this University, after its authentication and the voucher specimen (#16327) was retained in Prisco Bezerra He...

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“…In addition, B 1 receptors are mainly implicated in neurogenic inflammation processes. The B 1 antagonist des-Arg 9 ,leu 8 -BK has been reported to inhibit the capsaicin-induced mouse ear edema by modulation of neurogenic inflammation (Mantione and Rodriguez, 1990). B 1 antagonists also block inflammation-like hypotension and plasma protein infiltration of the intestinal wall, observed during mesenteric postischemic reperfusion in the anesthetized rat, presumably regulated by a neurogenic reflex response (Madeddu et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

SSR240612 [(2R)-2-[((3R)-3-(1,3-Benzodioxol-5-yl)-3-{[(6-methoxy-2-naphthyl)sulfonyl]amino}propanoyl)amino]-3-(4-{[2R,6S)-2,6-dimethylpiperidinyl]methyl}phenyl)-N-isopropyl-N-methylpropanamide Hydrochloride], a New Nonpeptide Antagonist of the Bradykinin B₁Receptor: Biochemical and Pharmacological Characterization

Gougat

Ferrari²,

Sarran³

et al. 2004

J Pharmacol Exp Ther

111

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The biochemical and pharmacological properties of a novel non-peptide antagonist of the bradykinin (BK) B 1 receptor, SSR240612 [(2R)-2-[((3R)The compound selectivity for B 1 versus B 2 receptors was in the range of 500-to 1000-fold. SSR240612 inhibited Lys 0 -desAr 9 -BK (10 nM)-induced inositol monophosphate formation in human fibroblast MRC5, with an IC 50 of 1.9 nM. It also antagonized des-Arg 9 -BK-induced contractions of isolated rabbit aorta and mesenteric plexus of rat ileum with a pA 2 of 8.9and 9.4, respectively. Antagonistic properties of SSR240612 were also demonstrated in vivo. SSR240612 inhibited desArg 9 -BK-induced paw edema in mice (3 and 10 mg/kg p.o. and 0.3 and 1 mg/kg i.p.). Moreover, SSR240612 reduced capsaicin-induced ear edema in mice (0.3, 3 and 30 mg/kg p.o.) and tissue destruction and neutrophil accumulation in the rat intestine following splanchnic artery occlusion/reperfusion (0.3 mg/kg i.v.). The compound also inhibited thermal hyperalgesia induced by UV irradiation (1 and 3 mg/kg p.o.) and the late phase of nociceptive response to formalin in rats (10 and 30 mg/kg p.o.). Finally, SSR240612 (20 and 30 mg/kg p.o.) prevented neuropathic thermal pain induced by sciatic nerve constriction in the rat. In conclusion, SSR240612 is a new, potent, and orally active specific non-peptide bradykinin B 1 receptor antagonist.Kinins are 9 to 11 amino acid peptides known to be important mediators of pain, inflammation, and cardiovascular homeostasis. They are released in injured tissues from kininogen by activation of plasma or tissue kallikreins (Bhoola et al., 1992). Kinins exert their biological activities via the activation of two subtypes of G-protein coupled receptors, denoted B 1 and B 2 receptors (Regoli and Barabe, 1980;Regoli et al., 1998). Bradykinin (BK) and Lys 0 -BK are natural endogenous agonists of bradykinin B 2 receptors, whereas their kininase I-hydrolyzed metabolites des-Arg 9 -BK and Lys 0 -des-Arg 9 -BK are specific agonists of bradykinin B 1 receptors. B 1 peptide antagonists were obtained by replacing the C-terminal Phe residue of agonists by Leu. Human and rabbit B 1 receptors have a higher affinity for Lys 0 -desArticle, publication date, and citation information can be found at

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A bradykinin (BK)₁ receptor antagonist blocks capsaicin‐induced ear inflammation in mice

Cited by 50 publications

References 10 publications

Profile of capsaicin‐induced mouse ear oedema as neurogenic inflammatory model: comparison with arachidonic acid‐induced ear oedema

Profile of capsaicin‐induced mouse ear oedema as neurogenic inflammatory model: comparison with arachidonic acid‐induced ear oedema

Topically Applied Diterpenoids from Egletes viscosa (Asteraceae) Attenuate the Dermal Inflammation in Mouse Ear Induced by Tetradecanoylphorbol 13-Acetate- and Oxazolone

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A bradykinin (BK)1 receptor antagonist blocks capsaicin‐induced ear inflammation in mice

Cited by 50 publications

References 10 publications

Profile of capsaicin‐induced mouse ear oedema as neurogenic inflammatory model: comparison with arachidonic acid‐induced ear oedema

Profile of capsaicin‐induced mouse ear oedema as neurogenic inflammatory model: comparison with arachidonic acid‐induced ear oedema

Topically Applied Diterpenoids from Egletes viscosa (Asteraceae) Attenuate the Dermal Inflammation in Mouse Ear Induced by Tetradecanoylphorbol 13-Acetate- and Oxazolone

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A bradykinin (BK)₁ receptor antagonist blocks capsaicin‐induced ear inflammation in mice