BRITISH JOURNAL OF PHARMACOLOGY英国药理学杂志
BRITISH JOURNAL OF PHARMACOLOGY(英文缩写 BRIT J PHARMACOL),ISSN 0007-1188,eISSN 1476-5381,中文译名:英国药理学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 9.473 | Q1 |
| 2022 | 7.300 | Q1 |
| 2023 | 6.800 | Q1 |
| 2024 | 7.700 | Q1 |
| 2025 | 7.500 | Q1 |
BRITISH JOURNAL OF PHARMACOLOGY 最新收录文献
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1. {"_":"Kininase I drives angiotensin II-induced hypertension through activation of the bradykinin B receptor.","sub":["1"]}
1. {"_":"激肽酶I通过激活缓激肽B受体驱动血管紧张素II诱导的高血压。","sub":["1"]}PMID:日期:2026-10-04Kininase I, comprising carboxypeptidase N (CPN) and carboxypeptidase M, regulates kinin activity and is up-regulated during injury, inflammation and immune activation. Under these conditions, kininase I converts bradykinin and kallidin into des-Arg kinins, primary endogenous agonists of the bradykinin B receptor (R). BR signalling promotes vasoconstriction and inflammatory responses in the pathogenesis of hypertension. The roles of kininase I in regulating kinin-dependent signalling and inter-system interactions that contribute to blood pressure control and hypertensive organ injury remain poorly defined. CPN knockout (CPNKO) and wild-type (WT) mice underwent chronic Ang II infusion to evaluate the role of CPN, and a separate cohort of WT mice were treated with the kininase I inhibitor Mergetpa alongside angiotensin (Ang) II to assess the effects of kininase I inhibition. Ang II in WT mice increased blood pressure and was accompanied by sympathetic overactivation, increased BR expression, cardiac remodelling, immune cell infiltration and complement activation. CPNKO mice exhibited attenuated Ang II-induced hypertension, reduced B receptor expression, decreased cardiac fibrosis and blunted sympathetic activation. Pharmacologic inhibition of kininase I with Mergetpa reduced Ang II-induced increases in blood pressure, limited BR up-regulation and suppressed complement activation and immune cell infiltration. These findings identify kininase I as a critical enzymatic regulator linking the renin angiotensin and kallikrein kinin systems and highlight a mechanism through which cardiovascular and immune signalling pathways interact to drive hypertension. These results position kininase I as a potential therapeutic target for the treatment of hypertension.
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2. {"_":"Targeted delivery of the CB receptor agonist JWH-133 via VCAM-1-functionalised nanoparticles attenuates atherosclerosis and reveals sex-specific therapeutic outcomes.","sub":["2"]}
2. {"_":"通过VCAM-1功能化纳米颗粒靶向递送CB受体激动剂JWH-133可减轻动脉粥样硬化并揭示性别特异性治疗结果。","sub":["2"]}PMID:日期:2026-10-04Atherosclerosis, a chronic inflammatory disease characterised by lipid accumulation and endothelial dysfunction, remains a leading cause of cardiovascular morbidity and mortality. While cannabinoid 2 (CB) receptor agonists show therapeutic promise in preclinical studies, their systemic application is hindered by poor bioavailability and off-target effects. Consequently, targeted delivery systems are essential to enhance therapeutic efficacy and mitigate adverse effects. This study presents a targeted nanotherapeutic strategy for localising the CB receptor agonist directly at atherosclerotic lesions. Poly(lactic-co-glycolic acid) (PLGA) nanoparticles (NPs), encapsulating the selective agonist JWH-133 and functionalised with a VCAM-1 binding peptide (VBP) for selective binding to vascular cell adhesion molecule-1 (VCAM-1) (VBP-JWH-133-NPs), were developed. In vivo experiments were conducted in both male and female apolipoprotein E-deficient (ApoE) mice to assess the anti-inflammatory and lipid-modulating effects of the nanotherapy. Serum lipid profiles, aortic plaque burden and key inflammatory markers were analysed. VBP-JWH-133-NPs significantly reduced foam cell-rich depositions and modulate systemic inflammatory markers in both sexes, demonstrating superior anti-atherogenic efficacy compared with free JWH-133. The therapeutic benefits are notably more pronounced in male mice, which exhibit greater initial plaque area and lipid deposition. These findings underscore the potential of VBP-JWH-133-NPs as an efficient and superior delivery system for cannabinoid therapies in atherosclerosis. By addressing sex as a biological variable, this approach offers a nuanced strategy for developing more effective and precise cardiovascular interventions.
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3. The medial prefrontal cortex-ventral tegmental area dopaminergic circuit regulates the pleasure of tactile contact by releasing dopamine in the nucleus accumbens.
3. 内侧前额叶皮层-腹侧被盖区多巴胺能环路通过在伏隔核释放多巴胺来调节触觉接触的愉悦感PMID:日期:2026-10-01Tactile contact during social interactions is believed to enhance the experience of pleasure. Dopaminergic neurons in the ventral tegmental area (VTA) are crucial for the regulation of pleasurable emotions. We aim to reveal the specific circuit mechanisms by which the VTA contributes to pleasure derived from tactile contact. Paradigms of social interaction in the presence of physical contact (SIPPC) and social interaction in the absence of physical contact (SIAPC) were established. The expression of c-fos in different brain regions was detected by immunofluorescence. A combination of behavioural tests, fibre-optic calcium imaging, chemogenetics, patch-clamp techniques and molecular biological methods were used to investigate the circuit mechanism mediating pleasure of tactile contact. Dopaminergic neurons in the VTA were implicated in triggering pleasurable emotions associated with SIPPC. Mechanistically, SIPPC promoted the disinhibition of presynaptic neurons and enhanced excitatory synaptic transmission. Furthermore, projections from the mPFC to VTA dopaminergic neurons were activated during SIPPC. Chemogenetic activation of the mPFC-VTA circuit increased SIPPC-induced pleasure, whereas its inhibition decreased it. SIPPC triggered dopamine release in the nucleus accumbens (NAc), where the inhibition of dopamine receptors (DR) can reverse the pleasure-promoting effect of mPFC-VTA circuit activation during SIPPC. Collectively, these findings elucidate the key roles and mechanisms by which VTA neurons receive projections from the mPFC and subsequently release dopamine in the NAc to regulate the pleasure induced by tactile contact, which provide new insights into the mechanisms underlying the association between tactile and social interaction.
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4. Tracking and understanding intra- and intercellular second messengers signalling in pharmacology.
4. 药理学中细胞内和细胞间第二信使信号的追踪与理解PMID:日期:2026-09-29该文献暂无摘要。
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5. Positive modulation of glucagon-like peptide 1 (GLP-1) receptor by endogenous haemorphins with implications in glucose metabolism and diabetes.
5. 内源性血啡肽对胰高血糖素样肽1（GLP-1）受体的正向调节及其在糖代谢和糖尿病中的意义PMID:日期:2026-09-29Haemorphins are known to target G protein-coupled receptors and their reduced serum levels were associated with diabetes and obesity. This is consistent with inhibitory action on dipeptidyl peptidase IV, controlling GLP-1 levels. The modulation of the GLP-1 receptor by haemorphins as a mechanism for regulating glucose homeostasis was investigated. The effect of LVV-haemorphin 7 (LVV-H7) on GLP-1 receptor was assessed in human embryonic kidney (HEK293) and rat insulinoma (INS-1 832/3) cells using bioluminescence resonance energy transfer, downstream signalling, cell viability, insulin synthesis experimental and computational ligand binding analysis. LVV-H7 has positive action on GLP-1 receptor occurring with GLP-1 but not orforglipron (LY3502970), indicating a peptide-peptide interaction, causing a left shift in GLP-1's dose responses. LVV-H7 also potentiated GLP-1-induced insulin expression and its protective effect against glucose-induced cytotoxicity. Moreover, LVV-H7 slightly reduced the GLP-1's association kinetics with no impact on its binding properties. Molecular docking supported by functional analysis showed the existence of a putative 'allosteric' binding site at the junction between the helical and the extracellular domains (ECDs) and highlighted the critical role of Trp6 of LVV-H7 and Ser31/Glu34/Arg299/Asp372/Arg380™of GLP-1 receptor. This also demonstrated that active GLP-1/GLP-1 receptor complex is required for the positive action of LVV-H7. LVV-H7 is active on the GLP-1 receptor-mediated metabolic pathways in pancreatic β-cells. This is consistent with reduced serum haemorphin levels in diabetes/obesity, suggesting implications in glucose homeostasis. This constitutes the first Class B GPCR modulated by haemorphins, illustrating the role of haemorphin-GPCR axis in physiology/pathophysiology.
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6. Structural and biochemical basis for retinol-binding protein 4 antagonism by tinlarebant.
6. 丁那雷班拮抗视黄醇结合蛋白4的结构与生化基础PMID:日期:2026-09-29Retinol-binding protein 4 (RBP4) is a member of the lipocalin superfamily that is connected to disease states such as insulin resistance, fatty liver disease and ocular disorders including Stargardt disease. Several retinoid and non-retinoid antagonists of this protein have been developed for potential clinical use, but none have yet received FDA approval. Tinlarebant, a derivative of the early lead RBP4 antagonist, A1120, was reported to slow macular lesion growth in Stargardt disease patients. However, its precise mechanism of RBP4 antagonism remains undisclosed. The binding of tinlarebant to RBP4 was studied with fluorescence spectroscopy and crystallography. The impact of tinlarebant occupancy in the RBP4 retinol-binding pocket on RBP4 complexation with transthyretin (TTR) was studied by size-exclusion chromatography. The impact of tinlarebant on plasma RBP4 levels was studied in mice. Fluorescence quenching assays demonstrate that tinlarebant competitively displaces retinol from holo-RBP4 with an IC of 8.75 ± 0.38 nM. The RBP4-tinlarebant complex fails to associate with transthyretin in vitro. Administration of single doses of tinlarebant to mice reduced plasma RBP4 levels by up to 93%. The crystal structure shows that tinlarebant impedes RBP4 association with transthyretin through both conformational and steric effects. Tinlarebant is a tight-binding RBP4 antagonist that lowers RBP4 plasma levels due to disruption of the RBP4- transthyretin interaction. The crystal structure shows that tinlarebant integrates multiple aspects of RBP4 interaction and antagonism found in its predecessors. Together, these data illuminate the pharmacology of a clinical inhibitor of the RBP4-retinol transport system.
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7. Dietary melatonin and its benefits on cardiovascular disease.
7. 膳食褪黑素及其对心血管疾病的益处PMID:日期:2026-09-25Cardiovascular disease remains the leading cause of mortality globally, with a disproportionate burden in low- and middle-income countries. Melatonin, a hormone primarily produced by the pineal gland, exhibits notable antioxidant, anti-inflammatory and immunomodulatory properties that may confer cardiovascular benefits. Importantly, melatonin is also found in a wide range of dietary sources, raising the possibility that regular consumption of melatonin-rich foods could offer a low-cost, accessible strategy to support cardiovascular health. This review summarises knowledge on dietary melatonin and evaluates its potential to provide cardiovascular benefits.
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8. Repositioning niclosamide and alectinib to inhibit the hyperphosphorylation of SARS-CoV-2's nucleocapsid protein.
PMID:日期:2026-09-24In the past two decades, three pathogenic coronaviruses, including SARS-CoV-2, spilled over from natural animal reservoirs into the human population. Upon entry into infected cells, the nucleocapsid (N) protein of coronavirus becomes heavily phosphorylated within its central Ser-Arg domain by host kinase GSK-3, which triggers genomic RNA unpackaging and facilitates its recruitment to the replication transcription complex. Although initially considered a promising antiviral strategy, inhibiting N hyperphosphorylation requires high concentrations of kinase inhibitor and is impractical to achieve by conventional pharmacological means. We investigated the effect of GSK-3 inhibition on SARS-CoV-2 replication in Calu-3 and Vero E6 cells. The dose-dependent effect of the GSK-3 inhibitor to block N hyperphosphorylation was examined in 293T cells heterologously expressing the viral protein. Liquid chromatography-tandem mass spectrometry analysis was performed to evaluate the phosphorylation profile of the purified N protein. GSK-3 inhibition delays the release of progeny virus from infected cells. N hyperphosphorylation relies on a complex, redundant priming mechanism and exhibits strong cooperativity, which together contribute to resistance against GSK-3 inhibitors. The N and N mutations-present in the delta and omicron variants of concern (VOCs), respectively-reduce the efficiency of GSK-3-mediated phosphorylation. We discovered a novel pharmacological tool combining niclosamide and alectinib that partially degrades GSK-3 and restores the sensitivity of N hyperphosphorylation to the clinically tested GSK-3 inhibitor, enzastaurin. This work provides the biochemical basis for a novel approach to treat COVID-19 by synergistically repositioning two FDA-approved drugs.
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9. Generative AI in pharmacology publishing: Detection is necessary; governance of disclosure and equity is the harder task.
9. 药理学出版中的生成式人工智能：检测是必要的；披露与公平的治理才是更艰巨的任务PMID:日期:2026-09-23该文献暂无摘要。
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10. RETRACTION: Implications and Hidden Toxicity of Cardiometabolic Syndrome and Early-Stage Heart Failure in Carfilzomib-Induced Cardiotoxicity.
10. 撤稿：卡非佐米诱导的心脏毒性中心脏代谢综合征和早期心力衰竭的影响及隐藏毒性PMID:日期:2026-09-22该文献暂无摘要。