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 factor5.07Show impact factor historyHide impact factor history
- 5-year impact4.90
- Cited half-life7.70
- Immediacy index1.29
- Article influence1.37
- 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
- Author can archive a pre-print version
- Author cannot archive a post-print version
- Some journals impose embargoes typically of 6 or 12 months, occasionally of 24 months
- no listing of affected journals available as yet
- See Wiley-Blackwell entry for articles after February 2007
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- Publisher copyright and source must be acknowledged with set statement ("The definitive version is available at www.blackwell-synergy.com ")
- Articles in some journals can be made Open Access on payment of additional charge
- 'Blackwell Publishing' is an imprint of 'Wiley-Blackwell'
- Classification yellow
Publications in this journal
- British Journal of Pharmacology 08/2013;
Article: Br J Pharmacol. 2013 Jun 4. doi: 10.1111/bph.12263. [Epub ahead of print] Antagonism of histamine H4 receptor exacerbates clinical and pathological signs of experimental autoimmune encephalomyelitis. Ballerini C, Aldinucci A, Luccarini I, Galante A, Manuelli C, Blandina P, Katebe M, Chazot PL, Masini E, Passani MB.[show abstract] [hide abstract]
ABSTRACT: Abstract BACKGROUND AND PURPOSE: The histamine H4 receptor has a primary role in inflammatory functions that has made it an attractive target for the treatment of asthma and refractory inflammation. These observations suggested a facilitating action on autoimmune diseases. However, little is known about the role of the H4 receptor in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). EXPERIMENTAL APPROACH: We used EAE induced by myelin oligodendrocyte glycoprotein (MOG35-55 ) in C57BL/6 female mice, as a model of multiple sclerosis. The histamine H4 receptor antagonist 5-chloro-2-[(4-methylpiperazin-1-yl)carbonyl]-1H-indole (JNJ7777120) was injected i.p. daily starting at day 10 post-immunisation (D10 p.i.). Disease severity was monitored by clinical and histopathological evaluation of inflammatory cells infiltrating into the spinal cord, anti-MOG35-55 antibody production, assay of T cell proliferation by [3 H]-thymidine incorporation, mononucleate cells phenotype by flow cytometry, cytokine production by ELISA assay, transcription factors quantification of mRNA expression. KEY RESULTS: Treatment with JNJ7777120 worsened the severity of EAE, increased inflammation and demyelination in the spinal cord of EAE mice, it increased IFN-γ expression in lymph nodes, whereas it suppressed IL-4 and IL-10, and augmented expression of the transcription factors Tbet , FOXP3 and IL-17 mRNA in lymphocytes. JNJ7777120 did neither affect proliferation of anti-MOG35-55 T cells, anti-MOG35-55 antibody production, nor mononucleate cell phenotype. CONCLUSIONS AND IMPLICATIONS: Our data show a detrimental effect of H4 receptor blockade in EAE. Given the interest in the development of H4 receptor antagonists as anti-inflammatory compounds, it is important to understand the role of the H4 receptor in immune diseases to anticipate clinical benefits and also predict possible detrimental effects.British Journal of Pharmacology 06/2013;
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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;
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ABSTRACT: BACKGROUND AND PURPOSE: Phosphodiesterase 4 (PDE4) inhibitors produce potent antidepressant-like and cognition-enhancing effects. However, their clinical utility is limited by the major side effect of emesis, which appears to be PDE4 isoform-specific. Although PDE4D subtype plays the pivotal role in these therapeutic profiles, it is also the primary subtype responsible for emesis. Therefore, the aim of present research was to investigate whether long-form PDE4D variants mediate antidepressant-like and cognition-enhancing effects, but are irrespective with emesis. EXPERIMENTAL APPROACH: In mice microinfused with lentiviral vectors that contained shRNA-mir hairpin structure targeting long-form PDE4Ds into bilateral prefrontal cortices, the tail-suspension and forced-swim tests were used to measure antidepressant-like effects; novel object recognition and Morris water-maze tasks were used to determine cognition-enhancing effects. The emetic potential was assessed by alpha2 adrenergic receptor-mediated anaesthesia, a surrogate measure of emesis. Intracellular cAMP signalling was analysed by time-resolved FRET immunoassay and Western-blot. Dendritic complexity was assessed by Golgi staining. KEY RESULTS: Microinfusions of lentiviral PDE4D-shRNA down-regulated PDE4D4 and PDE4D5, and imitated the antidepressant-like and cognition-enhancing effects of the prototypical PDE4 inhibitor rolipram. The behavioural effects were related to dendritic complexity and mediated by the increased cAMP signalling. In addition, these effects were not enhanced in the presence of rolipram. Finally, while rolipram shortened the duration of combined anaesthesia, RNA interference-mediated PDE4D knock-down in the prefrontal cortex did not. CONCLUSION AND IMPLICATIONS: These data suggest that long-form PDE4Ds, at least PDE4D4 and PDE4D5, may be the promising targets for the development of PDE4 variant-selective inhibitors as the new pharmacotherapies for depressive disorders and neurodegenerative diseases involving memory deficits.British Journal of Pharmacology 02/2013; 168(4):1001-1014.
- British Journal of Pharmacology 12/2012;
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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;
- British Journal of Pharmacology 01/2012; 165(5):1515-1525.
- British Journal of Pharmacology 01/2012;
- British Journal of Pharmacology 01/2011;
- British Journal of Pharmacology 01/2011; 162:929.
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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