Clinical and Experimental Pharmacology and Physiology最新文献

{"title":"Exploring the Protective Role and Regulation of Prdx6 in Cisplatin-Induced AKI","authors":"Xianzhe Li,&nbsp;Jinbo Yu,&nbsp;Shi Cheng,&nbsp;Yaqiong Wang,&nbsp;Xiaoqiang Ding","doi":"10.1111/1440-1681.70093","DOIUrl":"https://doi.org/10.1111/1440-1681.70093","url":null,"abstract":"<div>\u0000 \u0000 <p>Cisplatin (CDDP) is a widely used chemotherapeutic agent that induces nephrotoxicity by generating excessive reactive oxygen species (ROS), leading to oxidative stress, inflammation and apoptosis in renal proximal tubular cells. Peroxiredoxin 6 (Prdx6), an antioxidant enzyme, plays a crucial role in maintaining ROS homeostasis by degrading hydroperoxides; however, its role in CDDP-induced acute kidney injury (CIAKI) remains unclear. In this study, a CIAKI model was established using CDDP treatment in vivo (C57BL/6 mice) and in vitro (PTECs) with or without Prdx6 overexpression (Prdx6 OE). CDDP treatment significantly increased ROS levels, while Prdx6 OE attenuated oxidative stress, apoptosis and renal tubular damage. Furthermore, we found that Prdx6 expression was regulated by Nuclear factor erythroid 2-related factor 2 (Nrf2), suggesting a mechanistic link between Nrf2 and Prdx6 in CIAKI. These findings indicate that Prdx6 plays a protective role in CDDP-induced nephrotoxicity by modulating oxidative stress and apoptosis, and highlight its potential as a therapeutic target.</p>\u0000 </div>","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"53 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145555658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The ELF1/IGF2BP2/FAM111B Cascade Drives Colorectal Cancer Progression and Ferroptosis Resistance","authors":"Dian Yin,&nbsp;Lili Cao,&nbsp;Mei Hua,&nbsp;Ying Chen","doi":"10.1111/1440-1681.70090","DOIUrl":"10.1111/1440-1681.70090","url":null,"abstract":"<div>\u0000 \u0000 <p>Epigenetic dysregulation plays a critical role in colorectal cancer (CRC) progression. Our study investigated the role of FAM111B in tumorigenic phenotypes and ferroptosis in CRC and the mechanisms by which epigenetic alterations influence FAM111B expression. Bioinformatics analyses revealed FAM111B expression and predicted the association between IGF2BP2 and FAM111B or ELF1. The influence on cell phenotypes was determined by assessing cell proliferation, migration, apoptosis and ferroptosis. Mechanism analyses were performed using luciferase reporter and ChIP assays. Subcutaneous xenografts were used to evaluate the role in vivo. FAM111B, IGF2BP2 and ELF1 were upregulated in CRC tumours and cell lines. FAM111B downregulation inhibited cell proliferation and migration while inducing apoptosis and ferroptosis. IGF2BP2 increased FAM111B expression by stabilising its mRNA, and ELF1 transcriptionally upregulated IGF2BP2. Moreover, ELF1 modulated FAM111B expression through IGF2BP2. ELF1 knockdown suppressed cell proliferation and migration while triggering apoptosis and ferroptosis, which could be abolished by reintroduction of IGF2BP2 or FAM111B. Additionally, ELF1 depletion diminished the in vivo tumorigenicity of HCT116 cells. The ELF1/IGF2BP2/FAM111B cascade drives CRC progression and ferroptosis resistance. Targeting this cascade may provide a therapeutic avenue for CRC treatment.</p>\u0000 </div>","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"52 12","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145480973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-Term Anticoagulation and Outcomes of Head and Neck Cancer: Analysis of the US Nationwide Inpatient Sample","authors":"Chun-Feng Wu,&nbsp;Hang Huong Ling,&nbsp;Yun-Cong Zheng,&nbsp;Po-Hsu Su,&nbsp;Hsuan-Jen Shih,&nbsp;Che-Wei Ou,&nbsp;Shih-Ming Chen,&nbsp;Yu-Cheng Chang,&nbsp;Yen-Min Huang","doi":"10.1111/1440-1681.70087","DOIUrl":"https://doi.org/10.1111/1440-1681.70087","url":null,"abstract":"<div>\u0000 \u0000 <p>Venous thromboembolism (VTE) is a complication of head and neck cancer (HNC). However, the effectiveness of routine anticoagulation as a preventive measure and its impact on patient outcomes is unclear. The purpose of this study was to evaluate the association between long-term systemic anticoagulation and in-hospital outcomes of patients with HNC. Data of patients ≥ 20 years old with HNC treated from 2005 to 2018 were extracted from the US Nationwide Inpatient Sample (NIS) database. Associations between long-term systemic anticoagulation and in-hospital outcomes were assessed by the univariate and multivariable regression analyses. The study included 20 312 patients with a mean age of 63 years, and 72% were males. Among them, 5078 (25.0%) were on long-term systemic anticoagulation. After adjustment, the multivariable analysis indicated long-term systemic anticoagulation was significantly associated with decreased odds for in-hospital mortality (adjusted odds ratio [aOR] = 0.64, 95% confidence interval [CI]: 0.54–0.76, <i>p</i> &lt; 0.001), overall life-threatening events (aOR = 0.84, 95% CI: 0.78–0.92, <i>p</i> &lt; 0.001), acute myocardial infarction (aOR = 0.76, 95% CI: 0.59–0.97, <i>p</i> = 0.026), sepsis (aOR = 0.80, 95% CI: 0.71–0.90, <i>p</i> &lt; 0.001) and acute kidney injury (aOR = 0.86, 95% CI: 0.76–0.97, <i>p</i> = 0.015). Long-term systemic anticoagulation was significantly associated with elevated overall bleeding risk (aOR = 1.34, 95% CI: 1.17–1.54, <i>p</i> &lt; 0.001) but not intracerebral haemorrhage (ICH) (aOR = 1.65, 95% CI: 0.90–3.04, <i>p</i> = 0.107). In conclusion, in patients with HNC, long-term anticoagulation is associated with better in-hospital outcomes, and does not increase the risk of ICH; however, there is an increased risk of overall bleeding.</p>\u0000 </div>","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"52 12","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145470048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory Bowel Disease and Novel Cell Death: Bibliometric Analysis and Study Trend Projections Based on Burst Detection","authors":"Hui Ouyang,&nbsp;Jingling Su,&nbsp;Jiawen Lin,&nbsp;Shuping Li,&nbsp;Yuan Sui,&nbsp;Chenxi Xie,&nbsp;Mingcheng Huang","doi":"10.1111/1440-1681.70088","DOIUrl":"10.1111/1440-1681.70088","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), is a chronic relapsing gastrointestinal inflammatory disorder, whose underlying mechanisms remain elusive. Novel cell death modalities such as ferroptosis and pyroptosis are implicated in its pathogenesis. This study employed bibliometric analysis to elucidate research trends in IBD and novel forms of cell death.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 682 records were retrieved from the Web of Science Core Collection on 20 June 2024, using relevant keywords. Bibliometric analysis and visualisation were conducted with tools including Citespace, VOSviewer, the bibliometrix R package, Scimago Graphica, and an online bibliometric platform. Topic modelling was performed via the latent Dirichlet allocation (LDA) algorithm, and burst detection was applied to forecast emerging research trends.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Over the past 20 years, there has been a remarkable increase in research output and influence in this field. The number of publications grew exponentially after 2019, and the median impact factor of highly cited papers also showed an upward trend. China and the United States were the major contributors. Chinese Academy of Sciences and Zhejiang University had the highest publication volumes among institutions. Key authors like Zhang Caiying and Markus F. Neurath were identified. Nature, Cell, and Gastroenterology were the most influential journals. Research focus evolved from traditional inflammatory mechanisms to diverse cell death mechanisms. Ten themes were identified through topic modelling, with their significance changing over time. MeSH and gene/protein/pathway analyses highlighted the importance of necroptosis, ferroptosis, and pyroptosis. Biclustering analysis explored specific research topics, and 22 gene/pathway/protein named entities with significant research potential were identified by burst detection.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This is the first bibliometric analysis of novel cell death in the context of IBD. It offers a holistic overview of research dynamics, trends, and hotspots in this field, which can enhance the comprehension of the field modalities and offer valuable guidance for future research. Future studies should focus on the interactions between different cell death forms and accelerate the translation of basic research findings into clinical applications.</p>\u0000 </section>\u0000 </div>","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"52 12","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safety Evaluation of Nitroimidazole Antibiotics Based on the FAERS Database","authors":"Qian Wu,&nbsp;Fansheng Wu,&nbsp;Han Jiang,&nbsp;Ling Jiang,&nbsp;Xingfei Zhang,&nbsp;Chengjun Guo,&nbsp;Longjian Huang,&nbsp;Junlong Ma,&nbsp;Yun Kuang,&nbsp;Yuxia Xiang,&nbsp;Chengxian Guo","doi":"10.1111/1440-1681.70084","DOIUrl":"10.1111/1440-1681.70084","url":null,"abstract":"<div>\u0000 \u0000 <p>Nitroimidazole antibiotics, including metronidazole, tinidazole, and ornidazole, are widely used to treat anaerobic infections and parasitic diseases. Although their efficacy is well established, comprehensive safety profiles—particularly concerning rare adverse events—remain incompletely elucidated. This study aimed to systematically evaluate the safety signals of these drugs using the FDA adverse event reporting system (FAERS) database from 2014 to 2024. Disproportionality analyses were performed at the system organ class (SOC) and standardised MedDRA queries (SMQ) levels to identify associations between nitroimidazole antibiotics and adverse events. A total of 17,631 adverse event reports were analysed for metronidazole, tinidazole, and ornidazole, respectively. Females comprised the majority of reports (57.35%, 51.70%, and 61.11%, respectively), which may reflect the common use of these agents in gynaecological infections. Metronidazole was associated with the shortest median time to onset of adverse events (2.5 days), while tinidazole had the longest (5.5 days). At the SOC level, all three drugs showed positive associations with gastrointestinal, nervous system, and cardiac disorders. Ornidazole showed strong disproportionality signals for vascular (IC₀₂₅ = 18.46) and skin disorders (IC₀₂₅ = 17.46), while tinidazole was associated with weaker but notable signals for skin and blood disorders. Notably, SMQ-level analysis uncovered significant safety signals not currently emphasised in drug labelling, including acute pancreatitis, hepatic failure, fibrosis/cirrhosis, and tachyarrhythmias for tinidazole and ornidazole. These findings highlight the potential need for intensified clinical monitoring of hepatic and cardiac function during treatment with these antibiotics. Although limited by the nature of spontaneous reporting data, this study offers important insights into both established and emerging risks associated with nitroimidazole antibiotics, reinforcing the value of continuous pharmacovigilance to optimise patient safety.</p>\u0000 </div>","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"52 12","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145387606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PDZK1 Regulates the Stability and Function of ADRB2 to Prevent Vascular Remodelling in Hypertension","authors":"Haoran Zhang,&nbsp;Yan Meng,&nbsp;Dandan Li,&nbsp;Wenjing Zheng,&nbsp;Wenjie Bu,&nbsp;Zhiyu Shi,&nbsp;Chunnan Liu,&nbsp;Meng Zhao,&nbsp;Huiying Wang,&nbsp;Yufeng Bai,&nbsp;Liying Luo,&nbsp;Dechao Zhao,&nbsp;Jinyu Chi","doi":"10.1111/1440-1681.70085","DOIUrl":"10.1111/1440-1681.70085","url":null,"abstract":"<div>\u0000 \u0000 <p>In this study, we found that PDZK1, a scaffold protein, interacts with the β₂-adrenergic receptor (ADRB2) through its PDZ domains, stabilising ADRB2 by inhibiting its ubiquitination and proteasomal degradation. This study explored the PDZK1–ADRB2 interaction and its role in hypertension-induced vascular remodelling. Using PDZK1 knockout mice infused with angiotensin II, we found that PDZK1 deficiency further exacerbates angiotensin II-induced hypertension, vascular dysfunction, and vascular remodelling. Mechanistically, PDZK1 stabilises ADRB2 protein by preventing its ubiquitination and proteasomal degradation, thereby maintaining ADRB2-mediated vasodilation. Additionally, PDZK1 prevents ADRB2 internalisation and its interaction with β-arrestin, thereby inhibiting β-arrestin–mediated ERK activation and suppressing vascular smooth muscle cell (VSMC) phenotypic switching. This mechanism contributes to vascular protection under hypertensive conditions. Targeting the PDZK1/ADRB2 interaction may provide a novel therapeutic strategy for hypertension-related vascular complications.</p>\u0000 </div>","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"52 12","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145372369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial Oxidative Stress and Cardiac Dysfunction in TERT Deficient Progeria Mice","authors":"Zandong Zhou,&nbsp;Yunpeng Zhang,&nbsp;Rui Zhao,&nbsp;Daiqi Liu,&nbsp;Bingxin Xie,&nbsp;Qingling Zhang,&nbsp;Gary Tse,&nbsp;Feng Wang,&nbsp;Tong Liu","doi":"10.1111/1440-1681.70082","DOIUrl":"https://doi.org/10.1111/1440-1681.70082","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Heart failure (HF) is a major cause of hospitalisation in the elderly. Its incidence increases with aging and the presence of risk factors such as hypertension and diabetes. Aging-related myocardial fibrosis, characterised by alterations in the extracellular matrix and myocardial structure, leads to impairment of cardiac function. However, the specific mechanisms linking mitochondrial oxidative stress to cardiac remodelling in aging remain unclear.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Objective&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;To elucidate the mechanisms underlying aging-related ventricular electrical and structural remodelling and to determine the role of mitochondrial dysfunction in modulating aging-associated HF.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods and Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;We developed third-generation homozygous telomerase reverse transcriptase deficient (TERT&lt;sup&gt;−/−&lt;/sup&gt;) progeria mice to model accelerated aging. Compared to wild-type controls, these mice exhibited marked upregulation of aging-associated genes and proteins such as p53 in ventricular tissue. Echocardiographic analysis revealed significant reductions in left ventricular ejection fraction and fractional shortening, indicating both systolic and diastolic dysfunction. Histological staining showed increased interstitial fibrosis and inflammatory cell infiltration, which correlated with elevated expression of fibrosis markers including collagen type I and TGF-β. Electrocardiography and epicardial mapping demonstrated prolonged QRS duration and slowed ventricular conduction velocity. These findings, together with increased conduction heterogeneity, are indicative of electrical remodelling. Furthermore, RNA sequencing and biochemical assays identified upregulation of mitochondrial oxidative stress pathways and elevated levels of malondialdehyde and MnSOD, alongside disrupted mitochondrial ultrastructure and downregulation of mitochondrial dynamics-related proteins such as MFN2 and Drp1. These findings highlight the central role of mitochondrial dysfunction in driving structural and electrical cardiac remodelling in aging.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The findings demonstrate that third-generation TERT&lt;sup&gt;−/−&lt;/sup&gt; senescent mice exhibit significant cardiac impairments, including electrical remodelling, structural changes, and mitochondrial dysfunction, suggesting mitochondrial oxidative stress may be related to aging-related HF. These insights underscore the potential of targeting mitochondrial dysfunction for therapeutic strategies in aging-related HF. Collectively, these data demonstrate that telomerase deficiency drives cardiac structura","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"52 12","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145284550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combination of Tanshinone IIA and Matrine Alleviates Lipopolysaccharide-Induced Acute Lung Injury by Supressing Ferroptosis via Nrf2/HO-1 Pathway Activation","authors":"Huanqing Xiong,&nbsp;Yujuan Li,&nbsp;Jiaying Gao,&nbsp;Jian Chen,&nbsp;Gang Liu,&nbsp;Faguang Jin","doi":"10.1111/1440-1681.70072","DOIUrl":"10.1111/1440-1681.70072","url":null,"abstract":"<div>\u0000 \u0000 <p>Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening conditions that involve severe lung inflammation leading to respiratory failure. Tanshinone IIA (TIIA) and Matrine (MAT), two herbal medicinal compounds, have been reported to exhibit several similar pharmacological properties including anti-inflammatory, antioxidant, and anticancer effects. Although previous studies have reported the combined therapeutic efficacy of using two drugs in treating ALI, it remains unknown whether TIIA and MAT have any synergistic effect in alleviating ALI/ARDS. Therefore, this study investigated whether a combined therapy of TIIA and MAT has protective effects against lipopolysaccharide (LPS)-induced ALI and its mechanism of action using mouse and cell models. The results showed that the TIIA + MAT combination ameliorated ALI by reducing edema, tissue injury, and proinflammatory cytokine secretion. This therapy enhanced antioxidant defences, as indicated by upregulated GPX4 and SLC7A11 levels, decreased 4-HNE and ROS levels, and ferroptosis inhibition. Furthermore, TIIA + MAT promoted Nrf2 nuclear translocation, leading to increased HO-1 expression and an anti-oxidative response. These findings suggest that the combination of TIIA and MAT alleviates LPS-induced ALI by inhibiting ferroptosis via activation of the Nrf2/HO-1 pathway. Thus, the co-administration of TIIA and MAT may be an effective therapeutic strategy for ALI, potentially offering a novel clinical approach to mitigate ferroptosis and inflammation.</p>\u0000 </div>","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"52 11","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Health Education During Root Canal Therapy Reduces the Use of Antibiotics","authors":"Ting Yi,&nbsp;Fan Gu,&nbsp;Shengbo Liu,&nbsp;Qiaowen Li,&nbsp;Li Wang,&nbsp;Wei Yin","doi":"10.1111/1440-1681.70083","DOIUrl":"10.1111/1440-1681.70083","url":null,"abstract":"<div>\u0000 \u0000 <p>Although antibiotics can effectively control infectious diseases, overuse of antibiotics can cause problems such as drug resistance. Pulpitis and apical periodontitis are among the most common infectious diseases in humans. To alleviate the intense tooth pain, patients often self-administer antibiotics. To guide patients in managing pulpitis and apical periodontitis more effectively, we designed a Root Canal Treatment Health Education Form and provided personalised guidance on antibiotic use during the treatment period. From January 2024 to March 2025, a total of 272 patients participated in this project. Benefiting from health education, the proportion of antibiotic use was significantly lower compared to the control group. Both patients and healthcare professionals involved in this health education program held positive attitudes towards the intervention. Our experience suggested that health education should be actively promoted in the treatment of pulpitis and apical periodontitis.</p>\u0000 </div>","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"52 11","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145243525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Indole-3-Propionic Acid Improves Vascular Function in High-Fat Diet-Induced Obese Mice via eNOS","authors":"Shaying Yang,&nbsp;Zhiwei Wang,&nbsp;Xin Wen","doi":"10.1111/1440-1681.70081","DOIUrl":"10.1111/1440-1681.70081","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The gut microbiota-derived metabolite indole-3-propionic acid (IPA) has been implicated in vascular homeostasis; however, its role in mesenteric vascular function and blood pressure regulation under obese conditions remains unclear. This study aimed to investigate the effects of IPA on mesenteric vascular endothelial function and blood pressure in high-fat diet-induced obese (DIO) mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>C57BL/6 mice were fed a high-fat diet for 3 months to induce the DIO model. DIO mice were gavaged daily with IPA (20 mg/kg) for 6 weeks. At the end of the treatment, inflammatory markers and nitric oxide (NO) levels in primary mesenteric artery endothelial cells were assessed by qPCR and fluorescence staining, respectively. Vascular relaxation function of the mesenteric arteries was measured via wire myograph. Additionally, the immediate effect of IPA on blood pressure was monitored via the tail-cuff method following IPA injection.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The results demonstrated that IPA treatment significantly reduced the levels of inflammatory cytokines in the endothelial cells of DIO mice. IPA administration markedly increased NO levels in endothelial cells and enhanced the endothelium-dependent vasodilation of mesenteric arteries. Mechanistically, IPA enhanced the phosphorylation of endothelial nitric oxide synthase (eNOS) via the PI3K/Akt pathway, promoting the production and release of NO, thereby regulating blood pressure. This was further validated in eNOS^−/− mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study reveals the vascular protective effects of IPA in obesity, providing new insights for the treatment of obesity-related cardiovascular diseases.</p>\u0000 </section>\u0000 </div>","PeriodicalId":50684,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"52 11","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145243461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}