Compounds > (1-s--2s)-4-amino-n-(1--carbamoyl-2--phenylethyl)-2-(4---methyl-1---naphthalenesulfonylamino)butanamide

(1-s--2s)-4-amino-n-(1--carbamoyl-2--phenylethyl)-2-(4---methyl-1---naphthalenesulfonylamino)butanamide and Edema

(1-s--2s)-4-amino-n-(1--carbamoyl-2--phenylethyl)-2-(4---methyl-1---naphthalenesulfonylamino)butanamide has been researched along with Edema* in 1 studies

Other Studies

1 other study(ies) available for (1-s--2s)-4-amino-n-(1--carbamoyl-2--phenylethyl)-2-(4---methyl-1---naphthalenesulfonylamino)butanamide and Edema

Article	Year
Effects of the somatostatin receptor subtype 4 selective agonist J-2156 on sensory neuropeptide release and inflammatory reactions in rodents. British journal of pharmacology, 2006, Volume: 149, Issue:4 Substance P (SP) and calcitonin gene-related peptide (CGRP) released from capsaicin-sensitive sensory nerves induce local neurogenic inflammation; somatostatin exerts systemic anti-inflammatory actions presumably via sst4/sst1 receptors. This study investigates the effects of a high affinity, sst4-selective, synthetic agonist, J-2156, on sensory neuropeptide release in vitro and inflammatory processes in vivo.. Electrically-induced SP, CGRP and somatostatin release from isolated rat tracheae was measured with radioimmunoassay. Mustard oil-induced neurogenic inflammation in rat hindpaw skin was determined by Evans blue leakage and in the mouse ear with micrometry. Dextran-, carrageenan- or bradykinin-induced non-neurogenic inflammation was examined with plethysmometry or Evans blue, respectively. Adjuvant-induced chronic arthritis was assessed by plethysmometry and histological scoring. Granulocyte accumulation was determined with myeloperoxidase assay and IL-1beta with ELISA.. J-2156 (10-2000 nM) diminished electrically-evoked neuropeptide release in a concentration-dependent manner. EC50 for the inhibition of substance P, CGRP and somatostatin release were 11.6 nM, 14.3 nM and 110.7 nM, respectively. J-2156 (1-100 microg kg(-1) i.p.) significantly, but not dose-dependently, inhibited neurogenic and non-neurogenic acute inflammatory processes and adjuvant-induced chronic oedema and arthritic changes. Endotoxin-evoked myeloperoxidase activity and IL-1beta production in the lung, but not IL-1beta- or zymosan-induced leukocyte accumulation in the skin were significantly diminished by J-2156.. J-2156 acting on sst4 receptors inhibits neuropeptide release, vascular components of acute inflammatory processes, endotoxin-induced granulocyte accumulation and IL-1beta synthesis in the lung and synovial and inflammatory cells in chronic arthritis. Therefore it might be a promising lead for the development of novel anti-inflammatory drugs. Topics: Animals; Anti-Inflammatory Agents; Arthritis, Experimental; Butanes; Carrageenan; Dose-Response Relationship, Drug; Edema; Electric Stimulation; Inflammation; Lipopolysaccharides; Male; Membrane Proteins; Mice; Mice, Inbred BALB C; Mustard Plant; Naphthalenes; Neurogenic Inflammation; Neuropeptides; Plant Oils; Pulmonary Eosinophilia; Rats; Rats, Inbred Lew; Rats, Wistar; Receptors, Somatostatin; Sulfones; Trachea	2006

Article

Year

Effects of the somatostatin receptor subtype 4 selective agonist J-2156 on sensory neuropeptide release and inflammatory reactions in rodents.

British journal of pharmacology, 2006, Volume: 149, Issue:4

Substance P (SP) and calcitonin gene-related peptide (CGRP) released from capsaicin-sensitive sensory nerves induce local neurogenic inflammation; somatostatin exerts systemic anti-inflammatory actions presumably via sst4/sst1 receptors. This study investigates the effects of a high affinity, sst4-selective, synthetic agonist, J-2156, on sensory neuropeptide release in vitro and inflammatory processes in vivo.. Electrically-induced SP, CGRP and somatostatin release from isolated rat tracheae was measured with radioimmunoassay. Mustard oil-induced neurogenic inflammation in rat hindpaw skin was determined by Evans blue leakage and in the mouse ear with micrometry. Dextran-, carrageenan- or bradykinin-induced non-neurogenic inflammation was examined with plethysmometry or Evans blue, respectively. Adjuvant-induced chronic arthritis was assessed by plethysmometry and histological scoring. Granulocyte accumulation was determined with myeloperoxidase assay and IL-1beta with ELISA.. J-2156 (10-2000 nM) diminished electrically-evoked neuropeptide release in a concentration-dependent manner. EC50 for the inhibition of substance P, CGRP and somatostatin release were 11.6 nM, 14.3 nM and 110.7 nM, respectively. J-2156 (1-100 microg kg(-1) i.p.) significantly, but not dose-dependently, inhibited neurogenic and non-neurogenic acute inflammatory processes and adjuvant-induced chronic oedema and arthritic changes. Endotoxin-evoked myeloperoxidase activity and IL-1beta production in the lung, but not IL-1beta- or zymosan-induced leukocyte accumulation in the skin were significantly diminished by J-2156.. J-2156 acting on sst4 receptors inhibits neuropeptide release, vascular components of acute inflammatory processes, endotoxin-induced granulocyte accumulation and IL-1beta synthesis in the lung and synovial and inflammatory cells in chronic arthritis. Therefore it might be a promising lead for the development of novel anti-inflammatory drugs.

Topics: Animals; Anti-Inflammatory Agents; Arthritis, Experimental; Butanes; Carrageenan; Dose-Response Relationship, Drug; Edema; Electric Stimulation; Inflammation; Lipopolysaccharides; Male; Membrane Proteins; Mice; Mice, Inbred BALB C; Mustard Plant; Naphthalenes; Neurogenic Inflammation; Neuropeptides; Plant Oils; Pulmonary Eosinophilia; Rats; Rats, Inbred Lew; Rats, Wistar; Receptors, Somatostatin; Sulfones; Trachea

2006