European Journal of Pharmacology (EUR J PHARMACOL)
The European Journal of Pharmacology publishes full-length papers, short communications and rapid communications on the mechanisms of action of chemical substances affecting biological systems. The journal also considers short reviews (not exceeding 12 pages in print) intended to debate recent advances in rapidly developing fields that are within its scope.Full-length papers and short communications are grouped under the following headings: Behavioral pharmacology, Neuropharmacology and analgesia, Cardiovascular pharmacology, Pulmonary, gastrointestinal and urogenital pharmacology, Endocrine pharmacology, Immunopharmacology and inflammation, and Molecular and cellular pharmacology. Manuscripts submitted to the journal are accepted on the understanding that: (1) they are subject to editorial review, (2) they have not been and will not be published in whole or in part in any other journal, and (3) the recommendations from the declaration of Helsinki and the internationally accepted principles in the use of experimental animals have been adhered to.
- Impact factor2.52Show impact factor historyHide impact factor history
- WebsiteEuropean Journal of Pharmacology website
Other titlesEuropean journal of pharmacology (Online), EJP
Material typeDocument, Periodical, Internet resource
Document typeInternet Resource, Computer File, Journal / Magazine / Newspaper
- Author can archive a pre-print version
- Author can archive a post-print version
- Voluntary deposit by author of pre-print allowed on Institutions open scholarly website and pre-print servers
- Voluntary deposit by author of authors post-print allowed on institutions open scholarly website including Institutional Repository
- Deposit due to Funding Body, Institutional and Governmental mandate only allowed where separate agreement between repository and publisher exists
- Set statement to accompany deposit
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- Must link to journal home page or articles' DOI
- Publisher's version/PDF cannot be used
- Articles in some journals can be made Open Access on payment of additional charge
- NIH Authors articles will be submitted to PMC after 12 months
- Authors who are required to deposit in subject repositories may also use Sponsorship Option
- Pre-print can not be deposited for The Lancet
Publications in this journal
Article: Taurine inhibits increased MMP-2 expression in a model of oxidative stress induced by glutathione depletion in rabbit heart.[show abstract] [hide abstract]
ABSTRACT: Abstract Matrix metalloproteinase enzymes (MMPs) activated by oxidative stress are involved in the pathogenesis of cardiovascular diseases. Glutathione (GSH) plays an important protective role against oxidatively induced damage in mammalian tissues. We investigated the possible role of gelatinases and the effect of the semiessential amino acid 2-aminoethanesulfonic acid (taurine) in oxidatively induced damage by GSH depletion in rabbit cardiac tissues. Rabbits were treated with buthionine sulfoximine (BSO), an effective GSH-depleting compound. BSO treatment significantly reduced GSH and increased MDA (malondialdehyde) levels. BSO treatment caused significant increase in proMMP-2 levels. MMP-9 (pro and active) expressions were not found in either treated- or untreated heart tissues. TIMP-1(endogenous inhibitor of MMP-9) and MT-MMP1 (endogenous activator of MMP-2) were not affected by BSO. Immunoscoring showed that MMP-2 expression significantly increased in hearts from BSO treated group but MMP-9 antibody did not show any significant positive immunostaining from all groups. Type I procollagen and total collagen did not significantly alter in heart tissues from all treatment groups. Taurine restored the increased MDA and the diminished GSH levels by BSO treatment. Pro MMP-2 expression was prevented by taurine. These results suggest that MMP-2 is a major gelanitase in rabbit hearts under oxidative stress and pharmacological inhibition of MMP-2 activation by taurine could represent a useful strategy for the prevention and/or treatment of different cardiovascular disorders. Copyright © 2013. Published by Elsevier B.V.European Journal of Pharmacology 03/2013;
Article: COX-2-derived prostaglandins do not contribute to coronary flow regulation in diabetic rats: Distinct secretion patterns of PGI(2) and PGE(2).European Journal of Pharmacology 12/2012;
Article: Protective effect of 2-hydroxy-4-methoxy benzoic acid on testosterone induced benign prostatic hyperplasia in Wistar rats Mohd Ismail Ali, Hari Durga Prasad Kondreddi, B. Veeresh n Department of Pharmacology, G. Pulla Reddy College of Pharmacy, Osmania University, Hyderabad 500028, Andhra Pradesh, India. European Journal of Pharmacology 698 (2013) 397–403European Journal of Pharmacology 10/2012; 698(213):397 - 403.
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ABSTRACT: Prostaglandin E2 is produced in inflammatory responses via the cyclooxygenase pathway and regulates a variety of physiological and pathological reactions through four different receptor subtypes; EP1, EP2, EP3 and EP4. The role of the classical prostanoid receptors stimulated by prostaglandin I2 and thromboxane A2 in the blood circulation has been largely studied, whereas the other receptor such as EP activated by prostaglandin E2, have been recently shown to be also implicated. There is now increasing evidence suggesting an important role of EP3 and EP4 receptor subtypes in the control of the human vascular tone and remodeling of the vascular wall as well in platelet aggregation and thrombosis. These receptors are implicated in vascular homeostasis and in the development of some pathological situations, such us atherosclerosis, aneurysms and hypertension. The use of specific EP agonists/antagonists would provide a novel cardiovascular therapeutic approach. In this review, we discuss the role of prostaglandin E2 receptors in the control of human blood and vascular cells.European Journal of Pharmacology 09/2012;
Article: Antidepressant-like effect of etazolate, a cyclic nucleotide phosphodiesterase 4 inhibitor-an approach using rodent behavioral antidepressant tests batteryEuropean Journal of Pharmacology 06/2012;
European Journal of Pharmacology 01/2012;
Article: Drug discovery targeting human 5-HT2C receptors: Residues S3.36 and Y7.43 impact ligand-binding pocket structure via hydrogen bond formationEuropean Journal of Pharmacology 01/2011;
Article: Shukla D, Saxena S, Purushothaman Jayamurthy, Shrivastava K, Singh M, Shukla S, Malhotra VK, Mustoori S, Bansal A. (2011). Hypoxic preconditioning with cobalt ameliorates hypobaric hypoxia induced pulmonary edema in rat. Eur J Pharmacol. 10;656(1-3):101-9. (IF-2.52).European Journal of Pharmacology 01/2011;
Article: Effects of cytostatics activity is enhanced by DNA methyltransferase inhibitors in the colorectal cancer cell linesEuropean Journal of Pharmacology 01/2010; 627:26-32.
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ABSTRACT: Angiotensin IV has been shown to improve learning and memory in rodents. Strain dependent variation in murine behaviour, aminopeptidase activity and inhibitory effect of Angiotensin IV, structural variation in insulin regulated aminopeptidase (IRAP) and aminopeptidase N (ApN) and expression of the encoding genes were explored. Strain differences in the behavioural response to Angiotensin IV were observed, where CD mice were refractory. All strains showed inhibition of aminopeptidase activity by Angiotensin IV but CD mice displayed reduced endogenous aminopeptidase activity. No differences in the coding sequence of IRAP or ApN were found. RT-PCR analysis showed no difference in IRAP expression between strains but an increased expression of ApN was observed in CD mice. The lack of cognitive response of CD mice to Angiotensin IV cannot be explained through variation within IRAP sequence nor expression but the results highlight a potential role for ApN in the effects of Angiotensin IV.European Journal of Pharmacology 01/2010;
Article: Neuroprotective effect of 5,7,3',4',5'-pentahydroxy dihdroflavanol-3-O-(2''-O-galloyl)-beta-d-glucopyranoside, a polyphenolic compound in focal cerebral ischemia in rat.European Journal of Pharmacology 01/2010; 626:205-212.
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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