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Targeting CK1δ and CK1ε as a New Therapeutic Approach for Clear Cell Renal Cell Carcinoma. 靶向 CK1δ 和 CK1ε 作为透明细胞肾细胞癌的一种新疗法。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-07-17 DOI: 10.1159/000540182
Yu-Chen Lin, Ding-Ping Sun, Tsung-Han Hsieh, Chun-Han Chen

Introduction: Kidney cancer ranks as the ninth most common cancer in men and the fourteenth in women globally, with renal cell carcinoma (RCC) being the most prevalent type. Despite advances in therapeutic strategies targeting angiogenesis and immune checkpoints, the absence of reliable markers for patient selection and limited duration of disease control underline the need for innovative approaches. CK1δ and CK1ε are highly conserved serine/threonine kinases involved in cell cycle regulation, apoptosis, and circadian rhythm. While CK1δ dysregulation is reportedly associated with breast and bladder cancer progression, their role in RCC remains elusive. This study aimed to investigate the feasibility of CK1δ/ε as new therapeutic targets for RCC patients.

Methods: The relationship between CK1δ/ε and RCC progression was evaluated by the analysis of microarray dataset and TCGA database. The anticancer activity of CK1δ/ε inhibitor was examined by MTT/SRB assay, and apoptotic cell death was analyzed by flow cytometry and Western blotting.

Results: Our data demonstrate that the gene expression of CSNK1D and CSNK1E is significantly higher in clear cell RCC (ccRCC) tissues compared to normal kidney samples, which is correlated with lower survival rates in ccRCC patients. SR3029, a selective inhibitor targeting CK1δ/ε, significantly suppresses the viability and proliferation of ccRCC cell lines regardless of the status of VHL deficiency. Importantly, the inhibitor promotes the population of subG1 cells and induces apoptosis, and ectopically expression of CK1δ partially rescued SR3029-induced apoptosis in ccRCC cells.

Conclusion: These findings underscore the crucial role of CK1δ and CK1ε in ccRCC progression, suggesting CK1δ/ε inhibitors as new therapeutic options for ccRCC patients.

导言:肾癌在全球男性癌症中占第九位,在女性癌症中占第十四位,其中肾细胞癌(RCC)是最常见的类型。尽管针对血管生成和免疫检查点的治疗策略取得了进展,但由于缺乏用于选择患者的可靠标记物,且疾病控制时间有限,因此需要采用创新方法。CK1δ和CK1ε是高度保守的丝氨酸/苏氨酸激酶,参与细胞周期调控、细胞凋亡和昼夜节律。据报道,CK1δ失调与乳腺癌和膀胱癌的进展有关,但它们在RCC中的作用仍不明确。本研究旨在探讨CK1δ/ε作为RCC患者新治疗靶点的可行性:方法:通过分析微阵列数据集和TCGA数据库,评估了CK1δ/ε与RCC进展之间的关系。MTT/SRB试验检测了CK1δ/ε抑制剂的抗癌活性,流式细胞术和Western印迹分析了细胞凋亡:结果:我们的数据表明,与正常肾脏样本相比,透明细胞RCC(ccRCC)组织中CSNK1D和CSNK1E的基因表达明显升高,这与ccRCC患者较低的存活率相关。SR3029是一种靶向CK1δ/ε的选择性抑制剂,它能明显抑制ccRCC细胞系的活力和增殖,而与VHL缺乏的状态无关。重要的是,该抑制剂可促进亚 G1 细胞的数量并诱导细胞凋亡,异位表达 CK1δ 可部分挽救 SR3029 诱导的 ccRCC 细胞凋亡:这些发现强调了CK1δ和CK1ε在ccRCC进展中的关键作用,建议将CK1δ/ε抑制剂作为ccRCC患者的新治疗选择。
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引用次数: 0
Early Use of PCSK9 Inhibitors in the Prognosis of Patients with Acute Coronary Syndrome by Protecting Vascular Endothelial Function. 通过保护血管内皮功能,早期使用 PCSK9 抑制剂有助于急性冠状动脉综合征患者的预后。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-07-17 DOI: 10.1159/000540083
Linghao Xu, Yuanqi Wang, Yiqiong Wang, Liang Wang, Peizhao Du, Jing Cheng, Chunsheng Zhang, Tiantian Jiao, Lijian Xing, Md Sakibur Rahman Tapu, Haonan Jia, Jiming Li

Introduction: Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) has a protective effect on acute coronary syndrome (ACS). However, most studies have shown that this protective effect is based on a decrease in low-density lipoprotein cholesterol, while other mechanisms remain limited. This study aimed to determine whether PCSK9i can improve the prognosis of ACS patients by protecting endothelial function.

Methods: A total of 113 ACS patients were enrolled and randomly assigned to PCSK9i group (PCSK9i combined with statins) and control group (statins only). Blood lipids and endothelial function indicators were measured and analyzed 6 weeks before and after treatment. The effect of PCSK9i on the expression and secretion of endothelial function indicators in vascular endothelial cells were studied by cell experiments.

Results: After 6 weeks of treatment, endothelial function indicators such as nitric oxide (NO), thrombomodulin, intercellular cell adhesion molecule-1, endothelin-1, and flow-mediated vasodilation were significantly improved in PCSK9i group compared with control group. Only the changes of NO and von Willebrand factor were associated with blood lipid levels, whereas the changes of other endothelial function indicators were not significantly associated with blood lipid levels. PCSK9i reduced the incidence of major adverse cardiovascular events in patients with ACS compared to those in the control group. In cell experiments, PCSK9i treatment significantly ameliorated LPS induced endothelial injury in HUVECs.

Conclusion: PCSK9i can protect vascular endothelial function partly independently of its lipid-lowering effect and ameliorate the prognosis of patients with ACS within 6 weeks. This mechanism may involve heat shock transcription factor 1/heat shock proteins -related signaling pathways. Early use of PCSK9i in patients with ACS should be strongly considered in clinical practice.

简介Proprotein convertase subtilisin/kexin type 9 inhibitors(PCSK9i)对急性冠状动脉综合征(ACS)有保护作用。然而,大多数研究表明,这种保护作用是基于低密度脂蛋白胆固醇(LDL-C)的降低,而其他机制仍然有限。本研究旨在确定 PCSK9i 是否能通过保护内皮功能改善 ACS 患者的预后:共纳入113名ACS患者,随机分配到PCSK9i组(PCSK9i联合他汀类药物)和对照组(仅他汀类药物)。在治疗前后6周测量并分析血脂和内皮功能指标。通过细胞实验研究 PCSK9i 对血管内皮细胞内皮功能指标表达和分泌的影响:结果:治疗6周后,与对照组相比,PCSK9i组NO、TM、ICAM-1、ET-1和血流介导的血管舒张(FMD)等内皮功能指标明显改善。只有 NO 和 vWF 的变化与血脂水平相关,而其他内皮功能指标的变化与血脂水平无明显关联。与对照组相比,PCSK9i 降低了 ACS 患者的 MACE 发生率。在细胞实验中,PCSK9i能明显改善LPS诱导的HUVECs内皮损伤:结论:PCSK9i能保护血管内皮功能,部分独立于其降脂作用,并能在6周内改善ACS患者的预后。这一机制可能涉及与 HSF1/HSPs 相关的信号通路。临床实践中应积极考虑对 ACS 患者尽早使用 PCSK9i。
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引用次数: 0
Transcription Factor E2F8 Activates PDK1-Mediated DNA Damage Repair to Enhance Cisplatin Resistance in Lung Adenocarcinoma. 转录因子 E2F8 可激活 PDK1 介导的 DNA 损伤修复,从而增强肺腺癌对顺铂的耐药性。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-05-29 DOI: 10.1159/000537819
Hongliang Li, Junxia Sun, Haibo Hu, Yi Wang

Introduction: Cisplatin (DDP) is the commonest chemo drug in lung adenocarcinoma (LUAD) treatment, and DDP resistance is a significant barrier to therapeutic therapy. This study attempted to elucidate the impact of PDK1 on DDP resistance in LUAD and its mechanism.

Methods: Bioinformatics analysis was used to determine the expression and enriched pathways of PDK1 in LUAD tissue. Subsequently, E2F8, the upstream transcription factor of PDK1, was predicted, and the binding relationship between the two was analyzed using dual-luciferase and ChIP experiments. PDK1 and E2F8 levels in LUAD tissues and cells were detected via qRT-PCR. Cell viability, proliferation, and apoptosis levels were assayed by CCK-8, EdU, and flow cytometry experiments, respectively. Comet assay was used to assess DNA damage, and immunofluorescence was used to assess the expression of γ-H2AX. NHEJ reporter assay was to assess DNA repair efficiency. Western blot tested levels of DNA damage repair (DDR)-related proteins. Immunohistochemistry assessed the expression of relevant genes. Finally, an animal model was constructed to investigate the influence of PDK1 expression on LUAD growth.

Results: PDK1 was found to be upregulated in LUAD and enhanced DDP resistance by mediating DDR. E2F8 was identified as an upstream transcription factor of PDK1 and was highly expressed in LUAD. Rescue experiments presented that knocking down E2F8 could weaken the promotion of PDK1 overexpression on DDR-mediated DDP resistance in LUAD. In vivo experiments showed that knocking down PDK1 plus DDP significantly reduced the growth of xenograft tumors.

Conclusion: Our results indicated that the E2F8/PDK1 axis mediated DDR to promote DDP resistance in LUAD. Our findings lead to an improved treatment strategy after drug resistance.

简介顺铂(DDP)是肺腺癌(LUAD)治疗中最常用的化疗药物,DDP耐药是治疗的一大障碍。本研究试图阐明 PDK1 对 LUAD 中 DDP 耐药性的影响及其机制:方法:利用生物信息学分析确定 PDK1 在 LUAD 组织中的表达和富集途径。随后,预测了PDK1的上游转录因子E2F8,并利用双荧光素酶和ChIP实验分析了二者的结合关系。通过 qPCR 检测了 LUAD 组织和细胞中 PDK1 和 E2F8 的水平。细胞活力、增殖和凋亡水平分别通过 CCK-8、EdU 和流式细胞术实验进行检测。彗星试验用于评估 DNA 损伤,免疫荧光用于评估 γ-H2AX 的表达。NHEJ报告试验用于评估DNA修复效率。Western blot检测DNA损伤修复(DDR)相关蛋白的水平。免疫组化评估了相关基因的表达。最后,构建了一个动物模型来研究 PDK1 表达对 LUAD 生长的影响:结果:发现PDK1在LUAD中上调,并通过介导DDR增强了DDP抗性。E2F8被鉴定为PDK1的上游转录因子,并在LUAD中高表达。拯救实验表明,敲除E2F8可以削弱PDK1过表达对LUAD中DDR介导的DDP抗性的促进作用。体内实验表明,敲除 PDK1 加上 DDP 能显著降低异种移植肿瘤的生长:我们的研究结果表明,E2F8/PDK1轴介导的DDR促进了LUAD的DDP耐药性。结论:我们的研究结果表明,E2F8/PDK1轴介导的DDR促进了LUAD对DDP的耐药,我们的发现有助于改进耐药后的治疗策略。
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引用次数: 0
Erratum. 勘误表。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-01 Epub Date: 2023-10-05 DOI: 10.1159/000534214
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引用次数: 0
Recent Advances in the Therapeutic Potential of Sinomenine for Cancer Treatment. 西诺明治疗癌症潜力的最新进展。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-01 Epub Date: 2024-01-30 DOI: 10.1159/000536133
PanZhen Jiang, Aqeela Zahra, Xi Guo, Jianping Wu

Background: Cancer is a major cause of death worldwide. Although modern medicine has made strides in treatment, a complete cure for cancer remains elusive.

Summary: Utilization of medicinal plants in traditional medicine for the treatment of multiple diseases, including cancer, is a well-established practice. Sinomenine is an alkaloid extracted from a medicinal plant and has a diverse range of biological properties, including anti-oxidative, anti-inflammatory, and antibacterial effects. Sinomenine exhibits inhibitory effects on various types of tumor cells, including breast, lung, and liver cancers. The anticancer properties of sinomenine are believed to involve stimulation of apoptosis and autophagy as well as suppression of cell proliferation, invasion, and metastasis.

Key message: This review summarizes the current research on sinomenine's potential as an anticancer agent, which may contribute to the discovery of more effective cancer treatments.

背景:癌症是全球死亡的主要原因。摘要:在传统医学中利用药用植物治疗包括癌症在内的多种疾病是一种行之有效的做法。西诺明是从一种药用植物中提取的生物碱,具有多种生物特性,包括抗氧化、抗炎和抗菌作用。西诺明对乳腺癌、肺癌和肝癌等各类肿瘤细胞具有抑制作用。西诺明的抗癌特性被认为涉及刺激细胞凋亡和自噬,以及抑制细胞增殖、侵袭和转移:本综述总结了目前有关西诺明作为一种抗癌剂的潜力的研究,这可能有助于发现更有效的癌症治疗方法。
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引用次数: 0
Retraction Statement. 撤回声明。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-01 Epub Date: 2024-05-06 DOI: 10.1159/000539157
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引用次数: 0
Risk Factors for Potential Drug-Drug Interactions in Patients on Chronic Peritoneal Dialysis. 慢性腹膜透析患者潜在药物间相互作用的风险因素。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-01 Epub Date: 2024-03-12 DOI: 10.1159/000537968
Milorad Stojadinovic, Mirjana Lausevic, Iman Assi Milosevic, Radica Zivkovic Zaric, Tamara Kosta Jemcov, Ljiljana Komadina, Dejan Slavko Petrovic, Petar Djuric, Ana Bulatovic, Stefan Jakovljevic, Slobodan Jankovic

Introduction: The prevalence of potential drug-drug interactions (pDDIs) is becoming a major safety concern, as it has been previously linked to a significant number of adverse drug events and could have serious consequences for patients, including death. This is especially relevant for patients with chronic renal failure, as they are particularly vulnerable to drug-drug interactions. The aim of this study was to evaluate the prevalence and associated factors of pDDIs in patients receiving chronic peritoneal dialysis.

Methods: An observational, cross-sectional study was conducted on consecutive peritoneal dialysis patients attending four tertiary care hospitals for regular monthly examination. The primary outcome was the number of pDDIs identified using Lexicomp. Potential predictors were determined using multiple linear regression.

Results: Total number of patients included in the study was 140. The results showed that pDDIs were highly prevalent, especially in patients who use antiarrhythmics (p = 0.001), have diabetes mellitus (p = 0.001), recently started peritoneal dialysis (p = 0.003), or have higher number of prescribed drugs (p < 0.001). Number of prescribed drugs (p < 0.001) remained a significant predictor of high-risk pDDIs in addition to the female gender (p = 0.043).

Conclusion: Clinicians should be particularly cautious when prescribing multiple medications to high-risk patients, such as peritoneal dialysis patients, to mitigate the risk of drug-drug interactions and associated adverse health outcomes.

导言:潜在的药物相互作用(pDDIs)正在成为一个重大的安全问题,因为它曾与大量药物不良事件有关,并可能对患者造成严重后果,包括死亡。这与慢性肾衰竭患者尤其相关,因为他们特别容易受到药物相互作用的影响。本研究旨在评估慢性腹膜透析患者中 pDDIs 的发生率和相关因素:方法:对在四家三级医院接受每月定期检查的连续腹膜透析患者进行观察性横断面研究。主要结果是使用 Lexicomp 发现的 pDDIs 数量。采用多元线性回归法确定潜在的预测因素:研究共纳入 140 名患者。结果显示,pDDIs 的发病率很高,尤其是在使用抗心律失常药物(p=0.001)、患有糖尿病(p=0.001)、最近开始腹膜透析(p=0.003)或处方药较多(pConculsion)的患者中:总之,临床医生在为腹膜透析患者等高危患者开具多种药物处方时应特别谨慎,以降低药物间相互作用和相关不良健康后果的风险。
{"title":"Risk Factors for Potential Drug-Drug Interactions in Patients on Chronic Peritoneal Dialysis.","authors":"Milorad Stojadinovic, Mirjana Lausevic, Iman Assi Milosevic, Radica Zivkovic Zaric, Tamara Kosta Jemcov, Ljiljana Komadina, Dejan Slavko Petrovic, Petar Djuric, Ana Bulatovic, Stefan Jakovljevic, Slobodan Jankovic","doi":"10.1159/000537968","DOIUrl":"10.1159/000537968","url":null,"abstract":"<p><strong>Introduction: </strong>The prevalence of potential drug-drug interactions (pDDIs) is becoming a major safety concern, as it has been previously linked to a significant number of adverse drug events and could have serious consequences for patients, including death. This is especially relevant for patients with chronic renal failure, as they are particularly vulnerable to drug-drug interactions. The aim of this study was to evaluate the prevalence and associated factors of pDDIs in patients receiving chronic peritoneal dialysis.</p><p><strong>Methods: </strong>An observational, cross-sectional study was conducted on consecutive peritoneal dialysis patients attending four tertiary care hospitals for regular monthly examination. The primary outcome was the number of pDDIs identified using Lexicomp. Potential predictors were determined using multiple linear regression.</p><p><strong>Results: </strong>Total number of patients included in the study was 140. The results showed that pDDIs were highly prevalent, especially in patients who use antiarrhythmics (p = 0.001), have diabetes mellitus (p = 0.001), recently started peritoneal dialysis (p = 0.003), or have higher number of prescribed drugs (p &lt; 0.001). Number of prescribed drugs (p &lt; 0.001) remained a significant predictor of high-risk pDDIs in addition to the female gender (p = 0.043).</p><p><strong>Conclusion: </strong>Clinicians should be particularly cautious when prescribing multiple medications to high-risk patients, such as peritoneal dialysis patients, to mitigate the risk of drug-drug interactions and associated adverse health outcomes.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"147-155"},"PeriodicalIF":2.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140022475","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}
引用次数: 0
Impairment of Autophagy Mediates the Uric-Acid-Induced Phenotypic Transformation of Vascular Smooth Muscle Cells. 自噬损伤介导尿酸诱导的血管平滑肌细胞表型转化。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-01 Epub Date: 2023-11-27 DOI: 10.1159/000534929
Yan Lu, Hanlin Zhang, Min Han, Ping Wang, Liping Meng

Introduction: Hyperuricemia may be involved in the phenotypic transformation of vascular smooth muscle cells, thus promoting the occurrence of atherosclerosis, and autophagy may be one of the important links, but little is known about the specific molecular mechanism.

Methods: We established a mouse model of hyperuricemia and studied the relationship between changes in autophagy levels and the phenotypic transformation of muscle cells.

Results: Our study found that high uric acid levels promote the phenotypic transformation of muscle cells by inhibiting autophagy, thus enhancing their proliferation and migration abilities. If autophagy is restored, phenotypic transformation can be reversed by reducing the levels of the transcription factor Kruppel-like factor 4.

Conclusion: Uric acid may induce the phenotypic transformation of muscle cells and promote the occurrence of atherosclerosis by disrupting normal autophagy.

导读:高尿酸血症可能参与血管平滑肌细胞的表型转化,从而促进动脉粥样硬化的发生,自噬可能是其中的重要环节之一,但具体的分子机制尚不清楚。方法:建立小鼠高尿酸血症模型,研究自噬水平变化与肌肉细胞表型转化的关系。结果:我们的研究发现,高尿酸水平通过抑制自噬促进肌肉细胞的表型转化,从而增强肌肉细胞的增殖和迁移能力。如果自噬恢复,表型转化可以通过降低转录因子kruppel样因子4的水平来逆转。结论:尿酸可能通过破坏肌细胞正常自噬,诱导肌细胞表型转化,促进动脉粥样硬化的发生。
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引用次数: 0
Anti-Inflammatory Effects of Japanese Herbal Medicine Hochuekkito in a Mouse Model of Acute Exacerbation of Chronic Obstructive Pulmonary Disease. 日本草药 Hochuekkito 在慢性阻塞性肺病急性加重小鼠模型中的抗炎作用
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-01 Epub Date: 2024-02-12 DOI: 10.1159/000536348
Kensuke Fukuda, Hirotaka Matsuzaki, Yoshihisa Hiraishi, Naoya Miyashita, Takashi Ishii, Masaaki Yuki, Hideaki Isago, Hiroyuki Tamiya, Akihisa Mitani, Akira Saito, Taisuke Jo, Takahide Nagase

Introduction: The traditional Japanese herbal medicine hochuekkito (TJ-41) has been reported to ameliorate systemic inflammation and malnutrition in patients with chronic obstructive pulmonary disease (COPD). TJ-41 has also been known to have preventive effects against influenza virus infection. However, its role in the acute exacerbation of COPD (AECOPD) remains to be elucidated. Our previous study established a murine model of viral infection-associated AECOPD that was induced by intratracheal administration of porcine pancreatic elastase (PPE) and polyinosinic-polycytidylic acid [poly(I:C)]. Here, we used this model and investigated the effects of TJ-41 in AECOPD.

Methods: Specific pathogen-free C57BL/6J mice were used. A COPD model was induced by treating mice intratracheally with PPE on day 0. To generate the murine model of AECOPD, poly(I:C) was administered intratracheally following PPE treatment on days 22-24. Mice were sacrificed and analyzed on day 25. Mice were fed a diet containing 2% TJ-41 or a control diet.

Results: Daily oral intake of TJ-41 significantly decreased the numbers of neutrophils and lymphocytes in the bronchoalveolar lavage fluid (BALF), which was accompanied by decreased transcripts of CXC chemokines involved in neutrophil migration, viz., Cxcl1 and Cxcl2, in whole lung homogenates and reduced Cxcl2 concentration in BALF.

Conclusion: This study demonstrates the anti-inflammatory effects of TJ-41 in a mouse model of AECOPD, suggesting the effectiveness of TJ-41 for the management of COPD. Clinical investigations evaluating the therapeutic efficacy of TJ-41 in AECOPD would be meaningful.

简介据报道,日本传统草药 hochuekito(TJ-41)可改善慢性阻塞性肺病(COPD)患者的全身炎症和营养不良状况。TJ-41 还具有预防流感病毒感染的作用。然而,它在慢性阻塞性肺病(AECOPD)急性加重期的作用仍有待阐明。我们之前的研究建立了一个病毒感染相关的 AECOPD 小鼠模型,该模型是通过气管内注射猪胰弹性蛋白酶(PPE)和聚肌苷酸-聚胞苷酸 [poly(I:C)] 诱导的。在此,我们利用这一模型研究了 TJ-41 对 AECOPD 的影响:方法:使用特定的无病原体 C57BL/6J 小鼠。方法:使用特定的无病原体 C57BL/6J 小鼠,在第 0 天用 PPE 对小鼠进行气管内处理,诱导 COPD 模型。为了建立 AECOPD 小鼠模型,在第 22-24 天用 PPE 处理小鼠后,气管内注射聚(I:C)。小鼠在第 25 天被处死并进行分析。给小鼠喂食含有 2% TJ-41 的饮食或对照饮食:结果:每天口服 TJ-41 可显著减少支气管肺泡灌洗液(BALF)中的中性粒细胞和淋巴细胞数量,同时减少全肺匀浆中参与中性粒细胞迁移的 CXC 趋化因子(即 Cxcl1 和 Cxcl2)的转录本,并降低 BALF 中的 Cxcl2 浓度:本研究证明了 TJ-41 在 AECOPD 小鼠模型中的抗炎作用,表明 TJ-41 可有效治疗慢性阻塞性肺病。评估 TJ-41 在 AECOPD 中疗效的临床研究将非常有意义。
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引用次数: 0
Prolonged Proton Pump Inhibitor Use and Thrombohemorrhagic Risk in Essential Thrombocythemia and Polycythemia Vera Patients Treated with Long-Term Aspirin: A Pilot Study. 长期使用阿司匹林治疗的原发性血小板增多症和多发性红细胞症患者长期使用质子泵抑制剂与血栓性出血风险:一项试点研究。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-01 Epub Date: 2024-01-03 DOI: 10.1159/000535078
Ivan Krečak, Ljerka Pivac, Hrvoje Holik, Martina Morić Perić, Ivan Zekanović, Eva Čubrić, Marko Skelin, Marko Lucijanić

Introduction: Proton pump inhibitors (PPIs) are known to decrease the risk of gastrointestinal (GI) bleeding. However, concerns have been raised regarding the potential pharmacodynamic interactions of PPIs and antiplatelet drugs with respect to cardiovascular risk. Patients with BCR::ABL1-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia (ET), and polycythemia vera (PV) often suffer from peptic ulcer disease (PUD) and frequently receive low-dose aspirin due to an intrinsically high thrombotic risk.

Method: This retrospective multicenter study from a community setting investigated whether continuous PPI use may affect thrombohemorrhagic risk in ET and PV patients treated with long-term aspirin.

Results: Ninety-four aspirin-treated MPN patients (ET = 36, PV = 58) were included; median age was 69.5 years (range 21-92) and 40 (42.6%) were males. Nineteen (20.2%) patients continuously received PPIs and pantoprazole (n = 15, 78.9%) was the most frequently received PPI. PV phenotype (p = 0.085), male sex (p = 0.011), and prior thrombosis (p = 0.005) were associated with PPI use, whereas no correlations were found with respect to age, disease risk, splenomegaly, mutational status, constitutional symptoms, cardiovascular risk factors, cytoreductive treatment, or any of the blood cell counts (p > 0.050 for all analyses). The median follow-up time was 55.5 months; 19 (20.2%) thrombotic and 13 (13.8%) bleeding events occurred during this time. The use of PPIs was not associated with an increased risk of thrombosis (p = 0.158) or overall bleeding (p = 0.229) and none of the patients treated with PPIs experienced GI bleeding.

Conclusions: Considering that Helicobacter pylori infection and PUD are quite frequent in ET and PV patients, these preliminary results may provide some reassurance to physicians regarding the absence of thrombohemorrhagic risk associated with prolonged PPI use in MPN patients treated with long-term aspirin. Our observations may be even more important in the light of recent evidence suggesting suboptimal platelet inhibition in ET with once-daily when compared to twice- or triple-daily aspirin which may also cause more abdominal discomfort. Limitations of this study are its retrospective design, limited number of patients included, and the lack of pharmacodynamic and pharmacokinetic assessments.

导言:众所周知,质子泵抑制剂(PPIs)可降低胃肠道(GI)出血的风险。然而,人们对 PPIs 和抗血小板药物在心血管风险方面的潜在药效学相互作用表示担忧。BCR::ABL1阴性骨髓增殖性肿瘤(MPNs)、原发性血小板增多症(ET)和真性红细胞增多症(PV)患者通常患有消化性溃疡病(PUD),由于其本身具有较高的血栓风险,因此经常服用小剂量阿司匹林:这项社区多中心回顾性研究调查了持续服用 PPI 是否会影响长期服用阿司匹林的 ET 和 PV 患者的血栓出血风险:研究纳入了94名接受阿司匹林治疗的MPN患者(ET=36人,PV=58人);中位年龄为69.5岁(21-92岁),男性40人(42.6%)。19例(20.2%)患者持续服用PPIs,泮托拉唑(15例,78.9%)是最常服用的PPI。PV表型(p = 0.085)、男性性别(p = 0.011)和既往血栓形成(p = 0.005)与PPI的使用有关,而与年龄、疾病风险、脾脏肿大、突变状态、体征、心血管风险因素、细胞再生治疗或任何血细胞计数均无相关性(所有分析的p均为0.050)。中位随访时间为 55.5 个月;期间发生了 19 起(20.2%)血栓事件和 13 起(13.8%)出血事件。使用 PPIs 与血栓形成(p = 0.158)或总体出血(p = 0.229)风险的增加无关,使用 PPIs 治疗的患者中没有人发生消化道出血:考虑到幽门螺杆菌感染和 PUD 在 ET 和 PV 患者中十分常见,这些初步结果可以让医生放心,长期服用阿司匹林的 MPN 患者长期服用 PPI 不会导致血栓出血风险。最近有证据表明,与每天服用两次或三次阿司匹林相比,每天服用一次阿司匹林对 ET 的血小板抑制效果欠佳,而每天服用两次或三次阿司匹林可能会引起更多腹部不适,因此我们的观察结果可能更为重要。本研究的局限性在于其回顾性设计、纳入的患者人数有限以及缺乏药效学和药代动力学评估。
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引用次数: 0
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Pharmacology
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