Pharmacology最新文献

{"title":"Effects and safety of Ginkgo biloba extract on hyperlipidemia: a meta-analysis of randomised controlled trial.","authors":"Ke Wang, Yan Sun, Xuying Zhu, Liyu Tao, Xiaoyu Liang, Siyan Xu, Yiding Sun","doi":"10.1159/000552374","DOIUrl":"https://doi.org/10.1159/000552374","url":null,"abstract":"<p><strong>Introduction: </strong>Previous studies have explored the effect of Ginkgo biloba extract (Gbe) on hyperlipidemia; however, the results were inconclusive. We aimed to assess the efficacy and safety of Gbe on hyperlipidemia.</p><p><strong>Methods: </strong>Pubmed, Wanfang, China National Knowledge Infrastructure (CNKI) were searched until Dec 31, 2024. Mean difference was pooled using random-effects models.</p><p><strong>Results: </strong>Ten randomised controlled trials were included in our study. Compared with proprietary Chinese medicine, the effect of Gbe on hyperlipidemia was not statistically significant, including total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL), low density lipoprotein (LDL). Compared with western medicine, the effect of Gbe on HDL was statistically significant (MD = 0.14, 95% CI= 0.01, 0.28, I2 = 81.06%, P = 0.017), not on TC, TG and LDL. In the age-specific analysis, we found that the effect of Gbe on TC was statistically significant among 50-60 age group (MD = -0.43, 95% CI= -0.85, -0.01, I2 = 83.76%, P = 0.042). Notably, among participants aged ≤50 years, TG reduction is greater in the control group than in the Gbe group (MD = 0.12, 95% CI= 0.03, 0.21, I2 = 0.00%, P = 0.012). In the dose-specific analysis, the medium dose group of Gbe had a more significant reduction on TC and TG (TC: MD=-0.69, 95% CI=-1.02, -0.37, I2 = 51.3%, P < 0.001; TG: MD = -0.34, 95% CI = -0.53, -0.15, I2 = 0.00%, P = 0.001).</p><p><strong>Conclusions: </strong>Gbe demonstrates a greater therapeutic effect on HDL compared with Western medicine and shows non-inferiority to proprietary Chinese medicine in improving HDL levels. Gbe shows a significant therapeutic effect on TC levels among individuals aged 50-60 years and in the medium-dose group.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-18"},"PeriodicalIF":3.2,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856716","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":"Sappanone A targets TFEB to promote lysosomal autophagy and attenuate high glucose-induced myocardial injury.","authors":"Chenchen Zhang, Chuanqi Zhang, Caiyun Yang, Li Zhang","doi":"10.1159/000551971","DOIUrl":"https://doi.org/10.1159/000551971","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetic cardiomyopathy (DCM) involves myocardial injury under hyperglycemia, where impaired autophagy and oxidative stress play critical roles. This study explores whether Sappanone A (a natural compound) alleviates DCM by activating TFEB-mediated lysosomal autophagy.</p><p><strong>Methods: </strong>In vitro: H9c2 cardiomyocytes were injured with high glucose and treated with Sappanone A. Cell viability (CCK-8), apoptosis (flow cytometry), ROS (DCFHDA), and autophagy markers (LC3-II/I, p62, LAMP1 via WB/qPCR) were assessed. In vivo: STZ-induced DCM mice received Sappanone A (10 mg/kg/day, 8 weeks). Cardiac function (echocardiography), serum ANP/BNP (ELISA), histopathology (H&E/Masson), and autophagy flux (TFEB/LAMP1) were analyzed. TFEB-knockout models and chloroquine (CQ, autophagy inhibitor) validated mechanistic links.</p><p><strong>Results: </strong>Sappanone A dose-dependently enhanced HG-injured cardiomyocyte survival, reduced apoptosis and ROS, while upregulating TFEB nuclear translocatiandlysosomal function.In DCM mice, it improved ejection fraction, reduced fibrosis, and restored autophagic flux.These effects were abolished in TFEB-knockout models or with CQ co-treatment, confirming TFEB-dependent autophagy as the core mechanism.</p><p><strong>Conclusion: </strong>Sappanone A protects against DCM by activating TFEB-driven lysosomal autophagy, mitigating oxidative stress, and preserving cardiac function. It represents a novel therapeutic candidate for DCM.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-25"},"PeriodicalIF":3.2,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856799","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":"Tocilizumab Biosimilars Versus Reference Tocilizumab in Rheumatoid Arthritis: A Meta-Analysis of Pharmacokinetic Biosimilarity, Efficacy, Safety, and Immunogenicity.","authors":"Young Ho Lee, Gwan Gyu Song","doi":"10.1159/000552447","DOIUrl":"https://doi.org/10.1159/000552447","url":null,"abstract":"<p><strong>Introduction: </strong>To systematically evaluate the efficacy, safety, immunogenicity, and pharmacokinetics (PK) of tocilizumab biosimilars compared to reference tocilizumab (r-TCZ) in patients with rheumatoid arthritis (RA) and healthy volunteers.</p><p><strong>Methods: </strong>We searched PubMed, Embase, and Cochrane CENTRAL for phase I and III randomized controlled trials (RCTs) comparing tocilizumab biosimilars vs. r-TCZ. Primary outcomes included change from baseline in DAS28-ESR, ACR20/50/70 response rates, adverse events (AEs), serious AEs (SAEs), anti-drug antibody (ADA) positivity, and PK parameters (AUC0-inf, Cmax, and AUC0-last). Random-effects meta-analyses were performed using mean difference (MD), risk ratio (RR), and geometric mean ratio (GMR) with 95% or 90% confidence intervals (CIs). This systematic review and meta-analysis have been registered in PROSPERO (CRD420251270353).</p><p><strong>Results: </strong>Eight studies met the inclusion criteria, comprising 3 phase III RCTs (n=1,696 RA patients) and 5 phase I RCTs (n=1,363 healthy volunteers), for a total of 3,059 participants. In RA patients, biosimilars demonstrated equivalent efficacy to r-TCZ at week 24, with no significant differences in DAS28-ESR change (MD -0.06; 95% CI -0.19 to 0.06; I²=0%) or ACR20 response rates (RR 1.03; 95% CI 0.96-1.10; I²=0). Results for ACR50 and ACR70 were similarly balanced. Safety profiles were comparable (any AE: RR 1.01; 95% CI 0.94-1.08), as was immunogenicity (ADA positivity: RR 1.28; 95% CI 0.99-1.65). In healthy volunteers, PK biosimilarity was confirmed across intravenous and subcutaneous routes with pooled GMRs (90% CI) of 104.5% (101.2-107.9%) for AUC0-inf, 101.4% (98.5-104.4%) for Cmax, and 102.3% (97.8-106.9%) for AUC0-last; all pooled CIs lay entirely within the 80-125% regulatory acceptance range (I²≤35).</p><p><strong>Conclusion: </strong>Tocilizumab biosimilars exhibit therapeutic similarity in RA patients and pharmacokinetic biosimilarity in healthy volunteers compared to r-TCZ, with comparable safety and immunogenicity, supporting their use as credible, cost-effective alternatives in clinical practice.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-27"},"PeriodicalIF":3.2,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856776","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":"Efficacy and Safety of Avacopan in ANCA-Associated Vasculitis: A Meta-Analysis of Randomized Controlled Trials.","authors":"Young Ho Lee, Gwan Gyu Song","doi":"10.1159/000551892","DOIUrl":"https://doi.org/10.1159/000551892","url":null,"abstract":"<p><strong>Background: </strong>Avacopan, an oral C5a receptor antagonist, has been identified as a promising glucocorticoid-sparing agent in the management of ANCA-associated vasculitis (AAV). Although individual randomized controlled trials (RCTs) have indicated its therapeutic potential, there remains a need for comprehensive integration of efficacy and safety data to guide clinical decision-making.</p><p><strong>Methods: </strong>We performed a meta-analysis of three pivotal RCTs-CLASSIC (n = 42), CLEAR (n = 67), and ADVOCATE (n = 331)-including a total of 440 individuals diagnosed with AAV. Primary endpoints encompassed clinical response, sustained and early remission rates, changes in renal function, as well as safety outcomes such as serious adverse events, infections, organ toxicity, hematologic complications, and glucocorticoid-related adverse effects. Summary effect estimates were derived using risk ratios (RR), mean differences (MD), and 95% confidence intervals (CI). Study heterogeneity was quantified using the I² statistic and corresponding p-values.</p><p><strong>Results: </strong>Avacopan was associated with efficacy outcomes that were equivalent to or exceeded those achieved with standard-of-care regimens. Clinical response (RR = 1.08; 95% CI: 0.98-1.19) and early remission (RR = 2.85; 95% CI: 0.95-8.54) favored avacopan. Improvements in renal parameters, including eGFR and renal response, were consistent but modest. Notably, avacopan substantially decreased glucocorticoid-related adverse events (RR = 0.78; 95% CI: 0.70-0.87; p <0.0001), particularly the incidence of diabetes, psychiatric complications, and general GC toxicity. Avacopan did not result in any significant increase in serious infections, mortality, or treatment discontinuations.</p><p><strong>Conclusions: </strong>Avacopan represents a highly effective and safer option compared to traditional glucocorticoid-based regimens for AAV. The capacity to sustain disease remission with reduced steroid-associated harm highlights its potential utility in evolving vasculitis treatment strategies.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-20"},"PeriodicalIF":3.2,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634098","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":"3-Hydroxybutyrate Prevents Pulmonary Vein Arrhythmogenesis by Regulating Calcium/Calmodulin-Dependent Protein Kinase II Signaling and Oxidative Stress.","authors":"Chye-Gen Chin, Fong-Jhih Lin, Yao-Chang Chen, Yung-Kuo Lin, Yen-Yu Lu, Satoshi Higa, Yu-Hsun Kao, Shih-Ann Chen, Yi-Jen Chen","doi":"10.1159/000551614","DOIUrl":"https://doi.org/10.1159/000551614","url":null,"abstract":"<p><p>Introduction Atrial fibrillation is the most common sustained cardiac arrhythmia, primarily caused by arrhythmogenic activity within the pulmonary veins (PVs). Enhanced ketone body utilization can prevent heart failure by reducing inflammation and oxidative stress, factors crucial for atrial fibrillation pathogenesis. However, the role of ketone bodies in PV arrhythmogenesis remains unclear. This study investigated the effect of 3-hydroxybutyrate (3-OHB), the most abundant ketone body, on PV arrhythmogenesis and explored the underlying mechanisms. Methods Using conventional microelectrodes and the patch-clamp technique, we analyzed electrophysiological characteristics and ionic currents in isolated rabbit PV tissues and single PV cardiomyocytes. Results The effects of 3-OHB (10 mM) on reactive oxygen species (ROS) production, calcium homeostasis, and phosphorylated calcium/calmodulin-dependent protein kinase II (CaMKII) expression were analyzed through confocal microscopy and Western blotting. The results indicated that 3-OHB dose-dependently reduced PV spontaneous activity, contractility and diastolic tension. However, these effects were blocked by KN93 and AIP, a CaMKII inhibitor. Moreover, 3-OHB reduced late sodium and L-type calcium currents in PV cardiomyocytes; these effects were blocked by KN93 and AIP. Furthermore, 3-OHB reduced cytosolic ROS levels and phosphorylated CaMKII expression. Conclusion 3-OHB prevents PV arrhythmogenesis by modulating ionic currents, reducing ROS production, and regulating CaMKII signaling. Thus, 3-OHB holds promise as an antiarrhythmic agent.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-26"},"PeriodicalIF":3.2,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147491654","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":"Heterogeneity and Regulatory Mechanisms of ALK-Mutant and Wild-Type Epithelial Cells in Non-Small-Cell Lung Cancer: Single-Cell Transcriptomics and Chromatin Accessibility.","authors":"Yafu Zhou, Manni Yi, Jianhua Yan, Huiguo Chen, Jingsong Yang","doi":"10.1159/000550967","DOIUrl":"10.1159/000550967","url":null,"abstract":"<p><strong>Introduction: </strong>Anaplastic lymphoma kinase (ALK) mutations are key oncogenic drivers in non-small-cell lung cancer (NSCLC). Although ALK tyrosine kinase inhibitors (TKIs) elicit high initial response rates, relapse due to acquired resistance is common. Conventional approaches fail to resolve tumor heterogeneity and epigenetic control, necessitating multi-omic integration to dissect molecular differences between ALK-mutant and wild-type (WT) tumors.</p><p><strong>Methods: </strong>Single-cell RNA sequencing (scRNA-seq) and matched chromatin accessibility (scATAC-seq) data of 5 WT and 4 ALK-mutant NSCLC samples from GEO (GSE274934) were integrated. \"Seurat\" and \"Harmony\" packages in R were used for data preprocessing and batch correction. \"Monocle\" package reconstructed epithelial differentiation trajectories. \"CellChat\" package delineated cell-cell communication. \"Signac\" package integrated multiple omics data and analyzed the differentially accessible chromatin regions. Motif enrichment based on the JASPAR database identified key transcription factors. The role of CEACAM6 in the malignant progression of ALK-mutant-mutant NSCLC was assessed by qRT-PCR, CCK-8, colony formation, and wound-healing assays.</p><p><strong>Results: </strong>ALK-mutant epithelial cells exhibit disrupted differentiation trajectories, characterized by loss of SPINK1 expression and pan-expression of MARCKSL1. ALK-mutant cells relied on CEACAM5/6 signaling for communication; WT cells primarily engaged in multidirectional MIF interactions. ALK-mutant cells showed increased global chromatin accessibility. Motif analysis revealed enrichment of polycomb repressive complex (PRC) pathway components and EGR1 binding sites (survival/drug resistance-associated) in ALK-mutant cells, whereas WT cells specifically enriched KLF5, ZNF148, and GLIS3 motifs. In vitro, CEACAM6 expression was significantly upregulated in ALK-mutant compared to WT cells. CEACAM6 knockdown significantly inhibited cell proliferation and migration, and reduced p-AKT and EGR1 protein levels, indicating that CEACAM6 promotes malignant progression of ALK-mutant NSCLC through the AKT-EGR1 signaling axis.</p><p><strong>Conclusion: </strong>ALK mutations drive tumor stemness and drug resistance by blocking epithelial cell differentiation, activating CEACAM6-mediated signaling, enhancing chromatin accessibility, and remodeling the EGR1/PRC regulatory network. Targeting CEACAM6 and its downstream effector EGR1 may represent an effective strategy to overcome ALK-TKI resistance.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-21"},"PeriodicalIF":3.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444679","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":"Targeting Autophagy to Restore Intestinal Integrity in Sepsis: Resveratrol's NOX1/SIRT1-Mediated Protective Effect.","authors":"Wei Zhang, Jiang Yu, Zhongliang Shi, Yanna Jiao, Zhizhen Lai, Jiahua Chi, Jiayan Li, Jianbiao Meng","doi":"10.1159/000550966","DOIUrl":"10.1159/000550966","url":null,"abstract":"<p><strong>Introduction: </strong>A serious complication of sepsis that directly impacts patient outcomes is intestinal barrier disruption. Although the polyphenolic molecule resveratrol (RE) is well known for its anti-inflammatory and antioxidant properties, its specific role in targeting the NADPH oxidase 1 (NOX1)/sirtuin 1 (SIRT1) pathway to protect against sepsis-induced intestinal barrier failure remains unexplored. Therefore, this study aimed to comprehensively investigate this novel mechanism.</p><p><strong>Methods: </strong>The lipopolysaccharide (LPS)-treated Caco-2 cells and sepsis mouse models (cecal ligation and puncture) were utilized to assess the protective effects of RE. Quantitative reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay, histological analysis, immunohistochemistry, and Western blot were employed to examine inflammatory cytokine levels, autophagy markers, and intestinal barrier function. The roles of NOX1 and SIRT1 in RE-mediated protection were explored through NOX1 overexpression and related molecular analyses.</p><p><strong>Results: </strong>RE significantly improved survival rates in sepsis mice, reduced inflammatory cytokines, and restored intestinal barrier function. RE reversed the increase of NOX1 and the decrease of SIRT1 in sepsis. Histological analysis data showed that RE protected the intestinal structure, maintained the expressions of tight junction proteins, and alleviated intestinal damage. In LPS-treated Caco-2 cells, RE inhibited inflammation, promoted autophagy, and suppressed reactive oxygen species production. NOX1 overexpression partially offset the protective effects of RE.</p><p><strong>Conclusion: </strong>By modifying the NOX1/SIRT1 signaling pathway, RE protects against sepsis-induced intestinal barrier failure. These results underline that the NOX1/SIRT1 pathway is instrumental in autophagy and inflammation control and that RE may be a viable treatment approach for sepsis-related intestinal damage.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-21"},"PeriodicalIF":3.2,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147318127","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":"Wedelolactone: Unveiling the Multifaceted Anti-Inflammatory Potential.","authors":"Lu Zhang, Di Liu, Qiuyang Huang, Qingyu Zhang, Lingzhi Liu, Yuting Cui, Enkai Li, Kuilong Huang","doi":"10.1159/000550254","DOIUrl":"10.1159/000550254","url":null,"abstract":"<p><strong>Background: </strong>Wedelolactone (WED) is a polyphenolic compound with a coumarin skeleton isolated from marigold. Despite its wide application in traditional medicine, its mechanisms of action and safety profile require further investigation.</p><p><strong>Summary: </strong>The key contributions of this review lie in: (1) the first systematic integration of WED's multi-target mechanisms across diseases through the AMPK/NF-κB/NLRP3 network; (2) clarification of its dose-effect relationship (effective therapeutic window: 5-100 mg/kg) and toxicity thresholds; (3) proposal of clinical translation strategies, including nanodelivery systems to address bioavailability issues. Recent studies revealed novel mechanisms such as WED's inhibition of ferroptosis via GPX4 and modulation of the FXR-bile acid axis, demonstrating efficacy in acute lung injury and liver fibrosis.</p><p><strong>Key messages: </strong>This article provides a comprehensive framework integrating mechanistic insights and translational research for WED's clinical development.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-10"},"PeriodicalIF":3.2,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113955","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":"Escitalopram Oxalate Improved Insomnia by Targeting SLC6A4 to Regulate the Hypothalamic-Pituitary-Adrenal Axis.","authors":"Xin Gu, Jing An, Mingxue Zhang, Hongyan Zhang, Zhan Lou, Bu Wang","doi":"10.1159/000550304","DOIUrl":"10.1159/000550304","url":null,"abstract":"<p><strong>Introduction: </strong>Escitalopram oxalate (ESC) was extensively reported to improve insomnia in patients with depression/anxiety. The serotonin transporter gene (SLC6A4) was involved in regulating insomnia. However, it is still unclear whether ESC improves insomnia by regulating SLC6A4 expression. Therefore, this study aimed to investigate whether ESC improves insomnia by regulating SLC6A4 based on clinical and animal experiments.</p><p><strong>Methods: </strong>The clinical and animal experiments were involved in this study. For clinical experiments, after all 110 participants were divided into four groups, the portable sleep electroencephalogram monitor, HAMA₁₄ scale, and HAMD₂₄ scale were used to evaluate patients' sleep quality, anxiety, and depression. For animal experiments, after all 18 ICR male mice were randomly divided into three groups (n = 6), the sodium pentobarbital-induced sleeping test, locomotor activity test, elevated plus maze, and open field test were used to evaluate mice's sleep quality and anxiety- and depression-like behaviors. The H&E staining was used to determine pathological injuries in mice's hippocampal tissues. The ELISA kits were adopted to detect the 5-HT, norepinephrine (NE), gamma-aminobutyric acid (GABA), and glutamate (Glu) levels in the hypothalamus tissue and the corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol (CORT) levels in the serum. The PubChem, DrugBank, and Therapeutic Target Database were employed to predict the potential targets of ESC. The immunohistochemical staining and Western blot were applied to assay the SLC6A4, 5-HTR1A, and 5-HTR2A expression levels in the hippocampal tissues of mice.</p><p><strong>Results: </strong>ESC shortened the sleep latency, extended the sleep time, enhanced the sleep efficiency, and improved anxiety and depression in patients and mice. ESC mitigated the pathological injuries in mice's hippocampal tissues. ESC effectively regulated mice's neurotransmitter levels and hypothalamic-pituitary-adrenal (HPA) axis homeostasis, including upregulating 5-HT and GABA and downregulating NE, Glu, CRH, ACTH, and CORT. Moreover, SLC6A4 was predicted as the potential target of ESC. ESC prominently inhibited SLC6A4 expression (p < 0.001) and regulated 5-HTR1A and 5-HTR2A expression (p < 0.001) in hippocampal tissues.</p><p><strong>Conclusion: </strong>Taken together, ESC was suitable for treating insomnia in the clinic and improved insomnia by targeting SLC6A4 to regulate the HPA axis in mice.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-13"},"PeriodicalIF":3.2,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145966774","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":"Retraction Statement.","authors":"","doi":"10.1159/000549042","DOIUrl":"10.1159/000549042","url":null,"abstract":"<p><p>The article \"Tanshinone IIA Affects Autophagy and Apoptosis of Glioma Cells by Inhibiting Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway\" [Pharmacology. 2017;99(3-4):188-195. https://doi.org/10.1159/000452340] by Lijuan Ding, Shudong Wang, Weiyao Wang, Peng Lv, Donghai Zhao, Feier Chen, Tianjiao Meng, Lihua Dong and Ling Qi has been retracted by the Publisher and the Editor.After the publication of this article, concerns were raised about the integrity of some of the data presented. Specifically, similar features appear between the two panels \"FITC-A 740 Y-P\" and \"FITC-A Mixed\" in Figure 3b of the article. In addition, panels in Figure 3b of this article are the same as panels in Figure 3 of another article by different authors, published subsequently in a different journal [1], specifically:Figure 3b panel \"FITC-A Tan IIA\" is the same as Figure 3c of [1].Figure 3b panel \"FITC-A 740 Y-P\" is the same as Figure 3a of [1].Figure 3b panel \"FITC-A Mixed\" is the same as Figure 3b of [1].The authors did not respond to requests to comment on the concerns and provide the raw data within the given timeframe despite multiple attempts of contact. We contacted the authors' institution to request an investigation. However, we did not receive a response. Given the severity of the concerns raised, this article is being retracted. The authors have not responded to our correspondence regarding this retraction despite multiple attempts of contact.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"50"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145573658","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}