British Journal of Pharmacology (BRIT J PHARMACOL)
All aspects of experimental pharmacology including: Cellular and molecular pharmacology Biochemical pharmacology Neuroscience All aspects of general pharmacology Special Reports for rapid publication of important new results of special pharmacological significance The British Journal of Pharmacology is the leading 'original papers' publication in the field of general pharmacology.
- Impact factor4.41Show impact factor historyHide impact factor history
- WebsiteBritish Journal of Pharmacology website
Other titlesBritish journal of pharmacology, BJP, Proceedings of the British Pharmacological Society
Material typePeriodical, Internet resource
Document typeJournal / Magazine / Newspaper, Internet Resource
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Publications in this journal
Article: Systemic bile acid sensing by G protein-coupled bile acid receptor 1 (GPBAR1) promotes PYY and GLP-1 release.[show abstract] [hide abstract]
ABSTRACT: BACKGROUND AND PURPOSE: Nutrient sensing in the gut is believed to be accomplished through activation of G-protein coupled receptors expressed on enteroendocrine cells. In particular, L-cells located predominantly in distal regions of the gut secrete GLP-1 and PYY upon stimulation by nutrients and bile acids. The study was designed to address the mechanism of hormone secretion in L-cells stimulated by the bile acid receptor GPBAR1. EXPERIMENTAL APPROACH: A novel, selective, orally bioavailable, and potent GPBAR1 agonist, RO5527239, was synthesized in order to investigate L-cell secretion in vitro and in vivo in mice and monkey. In analogy to bile acids, RO5527239 was conjugated with taurine to reduce oral bioavailability yet retaining its potency. Using RO5527239 and tauro-RO5527239, the acute secretion effects on L-cells were addressed via different routes of administration. KEY RESULTS: GPBAR1 signalling triggers the co-secretion of PYY and GLP-1, and leads to improved glucose tolerance. The strong correlation of plasma drug exposure and plasma PYY levels suggests activation of GPBAR1 from systemically accessible compartments. In contrast to the orally bioavailable agonist RO5527239, we show that tauro-RO5527239 triggers PYY release only when applied intravenously. Compared to mice, a slower and more sustained PYY secretion was observed in monkeys. CONCLUSIONS AND IMPLICATIONS: Selective GPBAR1 activation elicits a strong secretagogue effect on L-cells, which primarily requires systemic exposure. We suggest that GPBAR1 is a key player in the intestinal proximal-distal loop that mediates the early phase of nutrient-evoked L-cell secretion effects.British Journal of Pharmacology 03/2013;
Article: Interleukin-33/ST2 signalling contributes to carrageenin-induced innate inflammation and inflammatory pain: role of cytokines, endothelin-1 and prostaglandin E(2).[show abstract] [hide abstract]
ABSTRACT: BACKGROUND AND PURPOSE: IL-33 signals through ST2 receptor and induces adaptive and innate inflammation. IL-33/ST2 is involved in adaptive inflammation-induced pain. Herein, it was investigated the contribution of IL-33/ST2-triggered mechanisms to carrageenin-induced innate inflammation. EXPERIMENTAL APPROACH: Carrageenin- and IL-33-induced inflammatory responses were addressed in balb/c (WT) and ST2 deficient ((-/-) ) mice as follows: oedema (analog caliper), myeloperoxidase activity (colorimetric assay), mechanical hyperalgesia (electronic version of von Frey filaments), cytokines levels (ELISA), PGE(2) (RIA), mRNA expression (quantitative PCR), drug treatments targeting leukocyte recruitment (fucoidin), TNFα (infliximab), CXCL1 (antibody anti-CXCL1), IL-1 (IL-1ra), endothelin ET(A) (clazosentan) and ET(B) (BQ788) receptors and cyclooxygenase (indomethacin). KEY RESULTS: Carrageenin injection increased ST2 and IL-33 mRNA expression and IL-33 production in paw skin samples. Carrageenin-induced paw oedema, hyperalgesia and myeloperoxidase activity were reduced in ST2(-/-) compared to WT mice. These effects were mimicked by IL-33 injection in the paw. Furthermore, IL-33-induced hyperalgesia was reduced by fucoidin suggesting a role for recruited leukocytes in its hyperalgesic effect. IL-33-induced hyperalgesia in naïve mice was reduced by treatments targeting TNF, CXCL1, IL-1, endothelin receptors and cyclooxygenase while carrageenin-induced ST2-dependent TNFα, CXCL1, IL-1β, IL-10 and PGE(2) production and preproET-1 mRNA expression. Combining IL-33 and carrageenin at doses that were ineffective as single treatment induced significant hyperalgesia, oedema, myeloperoxidase activity, and cytokine production in a ST2-dependent manner. CONCLUSIONS AND IMPLICATIONS: IL-33/ST2 signalling triggers the production of inflammatory mediators contributing to carrageenin-induced inflammation. These data reinforces the importance of IL-33/ST2 signalling as a target in innate inflammation and inflammatory pain.British Journal of Pharmacology 01/2013;
British Journal of Pharmacology 12/2012;
Article: The gasotransmitter hydrogen sulphide decreases Na(+) transport across pulmonary epithelial cells.[show abstract] [hide abstract]
ABSTRACT: Background and purpose: The transepithelial absorption of Na(+) in the lung is crucial for the maintenance of the volume and composition of epithelial lining fluid. The regulation of Na(+) transport is essential, since hypo- or hyperabsorption of Na(+) is associated with lung diseases such as pulmonary oedema or cystic fibrosis. This study investigated the effects of the gaseous signalling molecule hydrogen sulphide (H(2) S) on Na(+) absorption across pulmonary epithelial cells. Experimental approach: Ion transport processes were electrophysiologically assessed in Ussing chambers on H441 cells grown on permeable supports at air/liquid interface and on native tracheal preparations of pigs and mice. The effects of H(2) S were further investigated on Na(+) channels expressed in Xenopus oocytes and Na(+) /K(+) -ATPase activity in vitro. Membrane abundance of Na(+) /K(+) -ATPase was determined by surface biotinylation and western blot. Cellular ATP concentrations were measured colorimetrically, and cytosolic Ca(2+) concentrations were measured with Fura-2. Key results: H(2) S rapidly and reversibly inhibited Na(+) transport in all employed models. There was no effect on Na(+) channels, whereas Na(+) /K(+) -ATPase currents were decreased. Membrane abundance, metabolic or calcium-dependent regulation, as well as direct activity of the Na(+) /K(+) -ATPase, were not involved in the H(2) S-effects. H(2) S inhibited basolateral calcium-dependent K(+) channels, which consequently decreased Na(+) absorption by H441 monolayers. Conclusions and Implications: H(2) S impairs pulmonary transepithelial Na(+) absorption, mainly due to the inhibition of basolateral Ca(2+) -dependent K(+) channels. This data suggests that the H(2) S signaling system might represent a novel pharmacological target for modifying pulmonary transepithelial Na(+) transport. © 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.British Journal of Pharmacology 02/2012; doi: 10.1111/j.1476-5381.2012.01909.x.
Article: 22-Role of Adenosine Kinase in Diabetic Retinopathy. EL-sherbeny N, Naime Mohammad, Ahmad Saif ,Elsherbini Ahmed, Mamdouh El-Shishtawy, Ahmad Saif Fulzele Sadanand, Laila A. Eissa, Mamdouh El-Shishtawy and Liou Gregory. British Journal of Pharmacology. Pharmacology Dec-2012. 23-Reno-protective effect of NECA in diabetic nephropathy: implication of IL-18 and ICAM-1 Nehal El-sherbiny ,Khaled Hissen, Mahmoud Gabr,Mohamed El-Gyyar ,lailaA. Eissa, Mamdouh El-Shishtawy. Eur Cytokine Netw. September 2British Journal of Pharmacology 01/2012;
Article: Clinical pharmacology of analgesics assessed with human experimental pain models: Bridging basic and clinical research.British Journal of Pharmacology 01/2012;
Article: Cyclopeptide RA-V inhibits angiogenesis by down-regulating ERK1/2 phosphorylation in HUVEC and HMEC-1 endothelial cells[show abstract] [hide abstract]
ABSTRACT: BACKGROUND AND PURPOSE Anti-angiogenic agents have recently become one of the major adjuvants for cancer therapy. A cyclopeptide, RA-V, has been shown to have anti-tumour activities. Its in vitro anti-angiogenic activities were evaluated in the present study, and the underlying mechanisms were also assessed.EXPERIMENTAL APPROACH Two endothelial cell lines, human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (HMEC-1), were used. The effects of RA-V on the proliferation, cell cycle phase distribution, migration, tube formation and adhesion were assessed. Western blots and real-time PCR were employed to examine the protein and mRNA expression of relevant molecules.KEY RESULTS RA-V inhibited HUVEC and HMEC-1 proliferation dose-dependently with IC50 values of 1.42 and 4.0 nM respectively. RA-V inhibited migration and tube formation of endothelial cells as well as adhesion to extracellular matrix proteins. RA-V treatment down-regulated the protein and mRNA expression of matrix metalloproteinase-2. Regarding intracellular signal transduction, RA-V interfered with the activation of ERK1/2 in both cell lines. Furthermore, RA-V significantly decreased the phosphorylation of JNK in HUVEC whereas, in HMEC-1, p38 MAPK was decreased.CONCLUSIONS AND IMPLICATIONS RA-V exhibited anti-angiogenic activities in HUVEC and HMEC-1 cell lines with changes in function of these endothelial cells. The underlying mechanisms of action involved the ERK1/2 signalling pathway. However, RA-V may regulate different signalling pathways in different endothelial cells. These findings suggest that RA-V has the potential to be further developed as an anti-angiogenic agent.British Journal of Pharmacology 11/2011; 164(7):1883-1898.
Article: Structural determinants of allosteric antagonism at metabotropic glutamate receptor 2: mechanistic studies with new potent negative allosteric modulators.British Journal of Pharmacology 01/2011; 164:521.
Article: Molecular pharmacological profile of a novel thiazolinone-bases direct and selective 5-lipoxygenaseInhibitor”British Journal of Pharmacology 01/2011;
Article: Characterization of RO4583298 as a novel potent, dual antagonist with in vitro activity at tachykinin NK1 and NK3 receptors.British Journal of Pharmacology 01/2011; 162:929.
Article: 16alpha-Hydroxycleroda-3,13 (14)Z-dien-15,16-olide from Polyalthia longifolia: a safe and orally active antileishmanial agent.British Journal of Pharmacology 01/2010; 159:1143.
British Journal of Pharmacology 08/2009; 157(7):1142-53.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
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