Oral anti-inflammatory action of NPC 18884, a novel bradykinin B2 receptor antagonist

Saleh, Tânia S.F; Vianna, Rose Mari Jacobsen; Creczynski-Pasa, Tânia B.; Chakravarty, Sarvajit; Mavunkel, Babu; Kyle, Donald J.; Calixto, João B.

doi:10.1016/s0014-2999(98)00778-x

Cited by 13 publications

(17 citation statements)

References 31 publications

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“…The results of the present study confirmed and extended our previous results (Saleh et al 1998) and show that the novel non-peptide BK B 2 receptor antagonist, NPC 18884, administered intraperitoneally, produces significant and dose-dependent inhibition of acetic acid-and kaolin-induced abdominal constrictions in mice. On a nmol basis, NPC 18884 was 3.5-fold less potent than HOE 140 and 9.9-fold less potent than the pseudopeptide NPC 18521.…”

Section: Discussionsupporting

confidence: 92%

“…administration. Such results suggest the main participation of BK B 2 receptors in BK-induced nociceptive responses and confirm further the systemic anti-BK actions of NPC 18884 (Saleh et al 1998).…”

Section: Discussionsupporting

confidence: 79%

“…When compared with the second generation of BK B 2 receptor antagonists such as HOE 140, NPC 17731 and NPC 17761, and mainly with the pseudopeptide BK B 2 receptor antagonist NPC 18521, NPC 18884 was less potent but equally effective in inhibiting both phases of the pain response and the oedema formation after intraplantar injection of formalin. On the other hand, while the peptides or the pseudopeptide receptor antagonists formerly cited are not orally active (Corrêa and Calixto 1993;Corrêa et al 1996;De Campos et al 1996;Kyle 1995;Stewart 1995), as reported early in mice model of pleurisy (Saleh et al 1998), NPC 18884 given orally produced marked inhibition against both the early and the late phase of the formalin-induced licking, as well as formalin-induced oedema formation.…”

Section: Discussionmentioning

confidence: 99%

“…1), inhibited [ 3 H]bradykinin binding (K d =80±26 nmol) in CHO cell lines that express the human B 2 receptor. We have reported recently that NPC 18884 given either intraperitoneally or orally to mice produced a rapid onset, selective and potent inhibition of the inflammatory responses caused by BK and by carrageenan in the mice model of pleurisy (Saleh et al 1998). …”

Section: Introductionmentioning

confidence: 99%

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Oral antinociception and oedema inhibition produced by NPC 18884, a non-peptidic bradykinin B2 receptor antagonist

Campos

Alves

Ferreira

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

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This study investigates the antinociceptive and the oedema inhibition properties of the novel non-peptide bradykinin (BK) B2 receptor antagonist, NPC 18884. Given by i.p. or p.o. routes NPC 18884 produced graded and long-lasting (at least 2.5h and 5.0h, respectively, for i.p. and p.o. administration) inhibition of acetic acid-induced abdominal constrictions in mice, with mean ID50 values of 8.3 nmol/kg and 439.9 nmol/kg. NPC 18884 also inhibited kaolin-induced abdominal constrictions (44+/-9% and 48+/-3% of inhibition, for i.p. and p.o. routes, respectively). Given by i.p. or p.o. routes NPC 18884 attenuated both phases of formalin-induced licking, as well as formalin-induced oedema formation. At similar doses NPC 18884 produced significant inhibition of capsaicin-induced nociception. NPC 18884, like HOE 140 given i.p., prevented the nociception caused by BK with mean ID50 values of 0.85 nmol/kg and 0.44 nmol/kg, respectively. Given orally NPC 18884, but not HOE 140, caused graded inhibition of BK-induced nociception (mean ID50 value of 50 nmol/kg). In rats, NPC 18884 given i.p. prevented BK and carrageenan-induced hyperalgesia (mean ID50 values of 6 nmol/kg and 13 nmol/kg), without affecting the hyperalgesia induced by des-Arg9-bradykinin (DABK) or by prostaglandin E2 (PGE2). NPC 18884 given i.p. inhibited the mouse paw oedema induced by tyrosine8-bradykinin or by carrageenan, but had no effect on DABK-induced oedema in mice pre-treated with Escherichia coli endotoxin, or that induced by PGE2. Thus, the novel non-peptide BK B2 receptor antagonist NPC 18884 produces rapid onset, potent and relatively long-lasting oral antinociceptive and oedema inhibition properties. The anti-BK actions of NPC 18884 are quite selective towards the BK B2 receptor-mediated responses.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oral antinociception and oedema inhibition produced by NPC 18884, a non-peptidic bradykinin B2 receptor antagonist

Campos

Alves

Ferreira

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

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“…]octane chloride, 100 mg/kg) [37] or the neurokinin 2 (NK 2 ) receptor antagonist SR48968 ((S)-Nmethyl-N[4-(4-acetylamino-4-phenylpiperidino)-2-(3,4,-dichlorophenyl)butyl]benzamide, 1 mg/kg) [37] were administered i. v. immediately before the i. p. injection of supernatants (0.2 ml/cavity) from macrophages stimulated with SEA or substance P (20 nmol/cavity) [38].…”

Section: Pharmacological Investigation With Different Drugsmentioning

confidence: 99%

Mouse macrophages release a neutrophil chemotactic mediator following stimulation by staphylococcal enterotoxin type A

DeSouza

Hyslop

Franco‐Penteado

et al. 2001

Inflammation Research

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Objective and Design: To examine the role of macrophages in the neutrophil migration induced by staphylococcal enterotoxin type A (SEA) in mice. Materials and Methods: Peritoneal macrophages were harvested from male Swiss mice pre-treated with thioglycollate. After adhering to plastic tissue culture dishes, the cells were washed and incubated with RPMI or SEA (0.62 -2.5 mg/ml) and washed again prior to further incubation with RPMI alone. The medium was then collected, sterilized and assayed for promigratory activity in the mouse peritoneal cavity. Results: Mouse macrophage monolayers stimulated with SEA secreted a thermolabile neutrophil chemotactic component (MNCC-SEA) with a molecular mass > 100 kDa (by ultrafiltration). This release was dose-and time-dependent and was inhibited by dexamethasone but not by indomethacin or BW755C. Dexamethasone, indomethacin, BWA4C, BW755C, BN52021, cimetidine and SR48968 had no effect on the neutrophil migration induced by MNCC-SEA while capsaicin and SR140333 reduced this phenomenon. Conclusions: Macrophages play a key role in the neutrophil recruitment induced by SEA probably by releasing an MNCC-SEA that presumably induces neutrophil migration via a mechanism mediated by substance P.

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Passiflora alata and Passiflora edulis spray-dried aqueous extracts inhibit inflammation in mouse model of pleurisy

et al. 2007

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Oral anti-inflammatory action of NPC 18884, a novel bradykinin B2 receptor antagonist

Cited by 13 publications

References 31 publications

Oral antinociception and oedema inhibition produced by NPC 18884, a non-peptidic bradykinin B2 receptor antagonist

Oral antinociception and oedema inhibition produced by NPC 18884, a non-peptidic bradykinin B2 receptor antagonist

Mouse macrophages release a neutrophil chemotactic mediator following stimulation by staphylococcal enterotoxin type A

Passiflora alata and Passiflora edulis spray-dried aqueous extracts inhibit inflammation in mouse model of pleurisy

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