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Retraction Note: Chronic stress-mediated dysregulations in inflammatory, immune and oxidative circuitry impairs the therapeutic response of methotrexate in experimental autoimmune disease models. 备注:慢性应激介导的炎症、免疫和氧化回路失调损害了甲氨蝶呤在实验性自身免疫性疾病模型中的治疗反应。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-07 DOI: 10.1007/s00210-026-05088-0
Rishabh Chaudhary, Mohd Akhtar Azam, Bhavana Dowand, Alpana Singh, Mujeeba Rehman, Vipul Agarwal, Anand Kumar, Arjun Singh Kaushik, Sukriti Srivastava, Siddhi Srivastava, Vikas Mishra
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引用次数: 0
An integrative genomic analysis of angiogenesis in hepatocellular carcinoma: from canonical drivers to emerging biomarkers. 肝细胞癌血管生成的综合基因组分析:从典型驱动因素到新兴生物标志物。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-06 DOI: 10.1007/s00210-026-05052-y
Suryaa Manoharan, Viswaganesh Venkatesan, Ekambaram Perumal

Angiogenesis, the production of new blood capillaries from pre-existing vasculature, is an important mechanism necessary for cancer progression and metastasis. This process may be regulated by the balance of pro-angiogenic and anti-angiogenic factors. The disruption of this balance leads to the induction of angiogenesis. Thus, there is a high necessity to identify these angiogenesis-related genes. In this study, we have used GeneCards database to obtain a list of angiogenesis-related genes followed by construction of protein-protein interaction (PPI) network using STRING database. Out of 37 angiogenesis-related genes, a single-gene cluster containing 27 genes was identified using MCODE analysis. The top ten hub genes were identified as FGF2, HIF1A, VEGFC, VEGFA, MMP9, THBS1, MMP2, KDR, IL6, and NOS, which were further analyzed. FunRich application was used to perform gene enrichment analysis and identify top interactors by constructing an interaction map. PPI map of each individual hub gene was constructed using search tool for the retrieval of interacting genes/proteins (STRING) database. The expression levels of each individual hub gene in HCC (liver hepatocellular carcinoma-LIHC dataset) and normal tissue were analyzed using the gene expression profiling interactive analysis 2 (GEPIA2) portal. The prognostic value of the hub genes was analyzed using Kaplan-Meier survival plot. The translational-level expression was analyzed using the IHC section images from the Human Protein Atlas (HPA) database. Thus, targeting these factors for therapy, diagnosis, or prognosis could be a key strategies in the field of oncology.

血管生成,即从已有的血管系统中产生新的毛细血管,是癌症进展和转移的重要机制。这一过程可能受促血管生成因子和抗血管生成因子的平衡调节。这种平衡的破坏导致血管生成的诱导。因此,鉴定这些血管生成相关基因是非常必要的。本研究利用GeneCards数据库获取血管生成相关基因列表,利用STRING数据库构建蛋白-蛋白相互作用(protein-protein interaction, PPI)网络。在37个血管生成相关基因中,使用MCODE分析鉴定了包含27个基因的单基因簇。前10个中心基因分别为FGF2、HIF1A、VEGFC、VEGFA、MMP9、THBS1、MMP2、KDR、IL6和NOS。利用FunRich应用程序进行基因富集分析,并通过构建相互作用图谱来识别顶级相互作用因子。利用互作基因/蛋白检索工具(STRING)数据库构建各枢纽基因的PPI图谱。使用基因表达谱交互分析2 (GEPIA2)门户网站分析每个枢纽基因在HCC(肝肝细胞癌- lihc数据集)和正常组织中的表达水平。应用Kaplan-Meier生存图分析枢纽基因的预后价值。利用Human Protein Atlas (HPA)数据库中的IHC切片图像分析翻译水平的表达。因此,针对这些因素进行治疗、诊断或预后可能是肿瘤学领域的关键策略。
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引用次数: 0
Identification of key bioactive compounds of medicine-food homologous substances and their multi-target intervention effects in ulcerative colitis treatment. 药食同源物关键生物活性化合物鉴定及其治疗溃疡性结肠炎的多靶点干预作用。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-06 DOI: 10.1007/s00210-026-05057-7
Wenhan Wu, Jinjin Li, Jun Zhang, Zhen Huang

Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by relapsing mucosal inflammation. Medicine-food homologous (MFH) substances represent a promising source of therapeutic compounds. This study aimed to identify promising key MFH-derived bioactives for UC intervention. Transcriptomic datasets from GEO were analyzed to overlap differentially expressed genes (DEGs) between UC and controls with UC-related target genes from public disease databases, generating candidate genes for functional enrichment analysis. Bioactive compounds from 110 MFH substances were compiled via dual-database integration. Compound-protein interactions were predicted using GraphBAN, followed by drug-likeness and toxicity evaluations to identify candidate key compounds and their corresponding potential key genes. An MFH substance-compound-gene tripartite network was constructed. Molecular docking and molecular dynamics (MD) simulations were performed, and the expression of candidate key genes was assessed in an independent UC/control tissue dataset. We identified 266 candidate genes enriched in immune response, inflammation, and cell adhesion pathways. MOL008417 was prioritized as the candidate key compound, with CHRM3, CYP17A1, CYP3A5, MPO, and NOS1 prioritized as potential key genes. Network analysis highlighted Dangshen (Codonopsis root) as a key MFH substance. Docking suggested a feasible binding between MOL008417 and CHRM3 (- 5.3 kcal/mol), and MD simulations indicated complex stability. Gene expression analysis demonstrated significant CHRM3 upregulation and CYP3A5 downregulation in inflamed UC tissues compared with non-inflamed UC tissues and control samples. Our integrated computational workflow suggests that the MFH-derived compound MOL008417 may have multi-target potential for UC treatment through interactions with potential key genes. These predictive findings offer a mechanistic hypothesis for the development of MFH-based interventions and could inform the design of novel, UC therapeutics, pending future experimental validation.

溃疡性结肠炎(UC)是一种慢性炎症性肠病,其特征是反复发作的粘膜炎症。药食同源(MFH)物质是一种很有前景的治疗性化合物来源。本研究旨在确定有希望的关键mfh衍生生物活性物用于UC干预。对来自GEO的转录组学数据集进行分析,将UC和对照组之间的差异表达基因(DEGs)与公共疾病数据库中的UC相关靶基因重叠,生成用于功能富集分析的候选基因。通过双数据库整合,从110种MFH物质中筛选出生物活性化合物。使用GraphBAN预测化合物与蛋白质的相互作用,然后进行药物相似性和毒性评估,以确定候选关键化合物及其对应的潜在关键基因。构建了MFH物质-化合物-基因三方网络。进行分子对接和分子动力学(MD)模拟,并在独立的UC/对照组织数据集中评估候选关键基因的表达。我们确定了266个候选基因,这些基因在免疫反应、炎症和细胞粘附途径中富集。MOL008417被优选为候选关键化合物,CHRM3、CYP17A1、CYP3A5、MPO和NOS1被优选为潜在关键基因。网络分析显示党参是MFH的关键物质。对接表明,MOL008417与CHRM3之间的结合是可行的(- 5.3 kcal/mol), MD模拟显示了复杂的稳定性。基因表达分析显示,与非炎症UC组织和对照样本相比,炎症UC组织中CHRM3显著上调,CYP3A5显著下调。我们的综合计算工作流程表明,mfh衍生的化合物MOL008417可能通过与潜在关键基因的相互作用具有治疗UC的多靶点潜力。这些预测性发现为基于mfh的干预措施的发展提供了一个机制假设,并可以为新型UC治疗方法的设计提供信息,有待于未来的实验验证。
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引用次数: 0
Convallatoxin ameliorates fibroblast-like synoviocytes-mediated synovial inflammation and joint destruction in rheumatoid arthritis by targeting IDH1. 康allatoxin通过靶向IDH1改善类风湿关节炎中成纤维细胞样滑膜细胞介导的滑膜炎症和关节破坏。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-06 DOI: 10.1007/s00210-026-05083-5
Suling Liu, Huijuan Hu, Yu Kuang, Simin Chen, Kai Sun, Chenxi Peng, Ruiru Li, Fan Su, Liuqin Liang, Qian Qiu, Youjun Xiao, Hanshi Xu

Convallatoxin (CNT), a cardiac glycoside purified from a traditional Chinese herb Adonis amurensis Regel et Radde, has been reported to exert anti-inflammatory and antitumor effects. However, its therapeutic effect on rheumatoid arthritis (RA), a chronic inflammatory disorder, remains unexplored. Thus, this study aimed to investigate the impact of CNT on regulating key functions of fibroblast-like synoviocytes (FLS) from patients with RA, evaluate its therapeutic efficacy on collagen induced arthritis (CIA) mouse model and further elucidate the underlying molecular mechanisms. Cell viability, proliferation and apoptosis were assessed using CCK8, EdU and Annexin V-AF647/ PI assays, respectively. RA FLS migration and invasion were evaluated using wound healing assay, Transwell and Matrigel assays. mRNA and protein levels of proinflammatory cytokines and matrix metalloproteinases (MMPs) were analyzed by RT-qPCR and ELISA, respectively. Protein expression in RA FLS and synovial tissues was examined via Western blotting and immunohistochemistry. Furthermore, RNA sequencing was employed to identify the potential downstream targets of CNT. The in vivo therapeutic efficacy of CNT was investigated using a CIA mouse model. In vitro experiments demonstrated that CNT (7.5, 15 and 30 nM) dose dependently inhibited migration, invasion and expression of IL-6, CCL2, MMP-2 and MMP-13 of RA FLS, without affecting proliferation and apoptosis. In vivo study showed that CNT treatment (50ug/kg/d and 150ug/kg/d) attenuated synovial inflammation and joint destruction in mice with CIA. Mechanistically, IDH1 was identified as the potential downstream target of CNT in RA FLS. IDH1 expression was significantly elevated in RA FLS and RA synovial tissues. Moreover, both CNT treatment and IDH1 knockdown suppressed AKT and NF-κB p65 phosphorylation. CNT inhibits aggressive behavior and inflammatory response of RA FLS by inhibiting IDH1-mediated activation of the AKT and NF-κB signaling pathways. Our findings suggest that CNT may be a potential novel therapeutic agent for RA.

康纳通毒素(conallatoxin, CNT)是一种从中药阿多尼(Adonis amurensis Regel et Radde)中纯化的心脏糖苷,具有抗炎和抗肿瘤的作用。然而,它对类风湿关节炎(RA)的治疗作用,一种慢性炎症性疾病,仍未被探索。因此,本研究旨在探讨CNT对RA患者成纤维细胞样滑膜细胞(FLS)关键功能的调节作用,评估其对胶原诱导关节炎(CIA)小鼠模型的治疗效果,并进一步阐明其潜在的分子机制。分别采用CCK8、EdU和Annexin V-AF647/ PI检测细胞活力、增殖和凋亡。采用伤口愈合试验、Transwell试验和Matrigel试验评估RA FLS的迁移和侵袭。采用RT-qPCR和ELISA分别分析促炎细胞因子和基质金属蛋白酶(MMPs) mRNA和蛋白水平。Western blotting和免疫组织化学检测RA FLS和滑膜组织的蛋白表达。此外,RNA测序被用于鉴定碳纳米管的潜在下游靶点。采用CIA小鼠模型研究碳纳米管的体内治疗效果。体外实验表明,CNT(7.5、15和30 nM)剂量依赖性地抑制RA FLS的迁移、侵袭和IL-6、CCL2、MMP-2和MMP-13的表达,而不影响其增殖和凋亡。体内研究表明,CNT处理(50ug/kg/d和150ug/kg/d)可减轻CIA小鼠滑膜炎症和关节破坏。在机制上,IDH1被确定为RA FLS中CNT的潜在下游靶标。IDH1在RA FLS和RA滑膜组织中的表达显著升高。此外,CNT处理和IDH1敲除均抑制了AKT和NF-κB p65的磷酸化。CNT通过抑制idh1介导的AKT和NF-κB信号通路的激活,抑制RA FLS的侵袭行为和炎症反应。我们的研究结果表明,碳纳米管可能是一种潜在的新型RA治疗剂。
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引用次数: 0
Respiratory drugs and psychiatric adverse events in children and adolescents: a pharmacovigilance study based on the FAERS database. 儿童和青少年的呼吸药物和精神不良事件:基于FAERS数据库的药物警戒研究。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-06 DOI: 10.1007/s00210-026-05075-5
Jing Feng, Shujuan Zhao

The association between respiratory drugs (RDs) and pediatric psychiatric adverse events (pAEs) remains insufficiently characterized. We aimed to characterize pAEs associated with RDs use in pediatric patients. RD-related pAE reports were retrieved from the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) database. Analysis focused on pediatric patients aged 0 to 17 years. Disproportionality analysis was conducted using four algorithms, with a focus on anxiety disorders and symptoms, depressed mood disorders and disturbances, and suicidal and self-injurious behaviors. Descriptive and clinical outcome analyses were performed, along with subgroup analyses to explore potential risk differentials by age and gender. Among 6,994 cases of RD-related pAEs in pediatric patients, 16 drugs with positive signals were identified across all four algorithms, with antiallergics accounting for 75.00%. Montelukast was the most frequently reported drug (n = 6,168), primarily associated with anxiety (21.84%, reporting odds ratio [ROR] = 15.08), depression (15.86%, ROR = 12.90), and suicidal ideation (14.27%, ROR = 13.63). Promethazine demonstrated strong signals for intentional self-injury (62.99%, ROR = 127.36). The highest mortality rates were observed with hydroxyzine (50.94%) and caffeine (50.00%), while oxytetracycline (4/4, 100%) showed the highest proportions of life-threatening events. Montelukast generated signals in all age and gender groups, with the highest disproportionality observed in children aged 0 to 4 years. This study identifies statistical associations between RDs and pAEs in pediatric patients, particularly with montelukast and promethazine. The highest mortality rates were observed with hydroxyzine. These findings provide a foundation for further research but require confirmation through large-scale prospective studies.

呼吸系统药物(RDs)与儿童精神不良事件(pAEs)之间的关系仍未充分表征。我们的目的是表征与儿科患者使用rd相关的pAEs。与rd相关的pAE报告从美国食品和药物管理局不良事件报告系统(FAERS)数据库中检索。分析的重点是0至17岁的儿科患者。使用四种算法进行歧化分析,重点关注焦虑障碍和症状、抑郁情绪障碍和障碍以及自杀和自残行为。进行了描述性和临床结果分析,并进行了亚组分析,以探索年龄和性别的潜在风险差异。在6994例儿科患者rd相关pAEs中,4种算法共识别出16种阳性信号药物,其中抗过敏药占75.00%。孟鲁司特是最常报告的药物(n = 6168),主要与焦虑(21.84%,报告优势比[ROR] = 15.08)、抑郁(15.86%,ROR = 12.90)和自杀意念(14.27%,ROR = 13.63)相关。异丙嗪表现出故意自伤的强信号(62.99%,ROR = 127.36)。羟嗪(50.94%)和咖啡因(50.00%)的死亡率最高,土霉素(4/ 4,100 %)的死亡率最高。孟鲁司特在所有年龄和性别群体中产生信号,在0至4岁的儿童中观察到最高的不均衡。本研究确定了儿科患者rd和pAEs之间的统计学关联,特别是孟鲁司特和异丙嗪。羟嗪组死亡率最高。这些发现为进一步的研究提供了基础,但需要通过大规模的前瞻性研究来证实。
{"title":"Respiratory drugs and psychiatric adverse events in children and adolescents: a pharmacovigilance study based on the FAERS database.","authors":"Jing Feng, Shujuan Zhao","doi":"10.1007/s00210-026-05075-5","DOIUrl":"https://doi.org/10.1007/s00210-026-05075-5","url":null,"abstract":"<p><p>The association between respiratory drugs (RDs) and pediatric psychiatric adverse events (pAEs) remains insufficiently characterized. We aimed to characterize pAEs associated with RDs use in pediatric patients. RD-related pAE reports were retrieved from the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) database. Analysis focused on pediatric patients aged 0 to 17 years. Disproportionality analysis was conducted using four algorithms, with a focus on anxiety disorders and symptoms, depressed mood disorders and disturbances, and suicidal and self-injurious behaviors. Descriptive and clinical outcome analyses were performed, along with subgroup analyses to explore potential risk differentials by age and gender. Among 6,994 cases of RD-related pAEs in pediatric patients, 16 drugs with positive signals were identified across all four algorithms, with antiallergics accounting for 75.00%. Montelukast was the most frequently reported drug (n = 6,168), primarily associated with anxiety (21.84%, reporting odds ratio [ROR] = 15.08), depression (15.86%, ROR = 12.90), and suicidal ideation (14.27%, ROR = 13.63). Promethazine demonstrated strong signals for intentional self-injury (62.99%, ROR = 127.36). The highest mortality rates were observed with hydroxyzine (50.94%) and caffeine (50.00%), while oxytetracycline (4/4, 100%) showed the highest proportions of life-threatening events. Montelukast generated signals in all age and gender groups, with the highest disproportionality observed in children aged 0 to 4 years. This study identifies statistical associations between RDs and pAEs in pediatric patients, particularly with montelukast and promethazine. The highest mortality rates were observed with hydroxyzine. These findings provide a foundation for further research but require confirmation through large-scale prospective studies.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146125763","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
The protective effect of ambroxol against cyclophosphamide-induced acute kidney injury involves Nrf2/HO-1 signaling upregulation and suppression of oxidative and inflammatory damage. 氨溴索对环磷酰胺引起的急性肾损伤的保护作用涉及Nrf2/HO-1信号的上调和氧化和炎症损伤的抑制。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-06 DOI: 10.1007/s00210-025-04919-w
Reem S Alruhaimi, Emad H M Hassanein, Sulaiman M Alnasser, Hanan S Althagafy, Mostafa Sabry, Abdullatif A Ahmed, Ayman M Mahmoud

Cyclophosphamide (CP) is a widely used chemotherapeutic agent whose clinical efficacy is often limited by its side effects, including nephrotoxicity. Oxidative stress and inflammation are central to CP-induced acute kidney injury (AKI). Ambroxol (ABX), a clinically approved mucolytic agent, has demonstrated antioxidant and anti-inflammatory properties that may be repurposed for nephroprotection. This study investigated the protective effects of ABX against CP-induced nephrotoxicity in rats and explored the underlying molecular mechanisms. Adult male rats received ABX (20 mg/kg/day) orally for seven consecutive days, with CP (100 mg/kg, i.p.) given on the fifth day. CP administration resulted in significant renal dysfunction, as indicated by elevated serum creatinine, BUN, uric acid, and Kim-1 levels. Histopathological analysis revealed glomerular degeneration, tubular damage, collagen deposition, and iron accumulation. CP also induced oxidative stress, evidenced by increased MDA and decreased GSH, SOD, and catalase, along with upregulation of NF-κB, elevated TNF-α and IL-1β levels, and increased cleaved caspase-3 expression. ABX reduced MDA, enhanced antioxidant defenses, and suppressed NF-κB and pro-inflammatory cytokines. ABX attenuated apoptosis as evidenced by reduced caspase-3 expression and concurrently modulated redox-sensitive signaling by upregulating Nrf2 and HO-1 expression and activity while downregulating Keap-1. ABX showed in silico binding affinity toward NF-κB, Keap-1, and HO-1. In conclusion, these findings suggest that ABX confers nephroprotection against CP-induced injury primarily through its antioxidant, anti-inflammatory, and anti-apoptotic actions, partly via modulation of the Keap-1/Nrf2/HO-1 pathway. These findings support potential repurposing of ABX as a nephroprotective adjuvant during CP chemotherapy and warrant further clinical investigation.

环磷酰胺(Cyclophosphamide, CP)是一种广泛使用的化疗药物,其临床疗效往往受到其副作用(包括肾毒性)的限制。氧化应激和炎症是cp诱导的急性肾损伤(AKI)的核心。氨溴索(ABX)是一种临床批准的黏液溶解剂,具有抗氧化和抗炎特性,可能被重新用于肾脏保护。本研究探讨了ABX对cp所致大鼠肾毒性的保护作用,并探讨其分子机制。成年雄性大鼠口服ABX (20 mg/kg/d),连续7天,第5天给予CP (100 mg/kg,每日1次)。CP给药导致明显的肾功能障碍,如血清肌酐、BUN、尿酸和Kim-1水平升高所示。组织病理学分析显示肾小球变性、小管损伤、胶原沉积和铁积累。CP还可诱导氧化应激,表现为MDA升高,GSH、SOD和过氧化氢酶降低,NF-κB上调,TNF-α和IL-1β水平升高,cleaved caspase-3表达升高。ABX降低MDA,增强抗氧化防御,抑制NF-κB和促炎细胞因子。ABX通过降低caspase-3的表达来减弱细胞凋亡,并通过上调Nrf2和HO-1的表达和活性,同时下调Keap-1来调节氧化还原敏感信号。ABX对NF-κB、Keap-1和HO-1具有硅结合亲和力。总之,这些研究结果表明,ABX主要通过其抗氧化、抗炎和抗凋亡作用,部分通过调节Keap-1/Nrf2/HO-1通路,对cp诱导的肾损伤起到保护作用。这些发现支持ABX在CP化疗期间作为肾保护佐剂的潜在用途,并需要进一步的临床研究。
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引用次数: 0
Correction to: Associations of sphingosine‑1‑phosphate with soluble P‑selectin and adverse clinical outcome in patients with cerebral ischemia with and without acetylsalicylic acid treatment. 修正:在接受和不接受乙酰水杨酸治疗的脑缺血患者中,鞘氨醇- 1 -磷酸与可溶性P选择素的关系和不良临床结果。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-06 DOI: 10.1007/s00210-026-05049-7
Nils-Ole Gloyer, Eileen Moritz, Laura Schwieren, Ulrike Meyer, Götz Thomalla, Günter Daum, Tim Magnus, Rainer Böger, Chi-Un Choe, Bernhard H Rauch, Edzard Schwedhelm
{"title":"Correction to: Associations of sphingosine‑1‑phosphate with soluble P‑selectin and adverse clinical outcome in patients with cerebral ischemia with and without acetylsalicylic acid treatment.","authors":"Nils-Ole Gloyer, Eileen Moritz, Laura Schwieren, Ulrike Meyer, Götz Thomalla, Günter Daum, Tim Magnus, Rainer Böger, Chi-Un Choe, Bernhard H Rauch, Edzard Schwedhelm","doi":"10.1007/s00210-026-05049-7","DOIUrl":"https://doi.org/10.1007/s00210-026-05049-7","url":null,"abstract":"","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146132150","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
Leonurine alleviates DSS-induced colitis in mice by activating the PINK1/Parkin-mediated mitophagy pathway: an integrated network pharmacology and experimental validation study. Leonurine通过激活PINK1/ parkinson介导的线粒体自噬通路减轻dss诱导的小鼠结肠炎:综合网络药理学和实验验证研究
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-05 DOI: 10.1007/s00210-026-05058-6
Tingting Cao, Juan Zhang, Wei Song, Guozhong Ji, Honggang Wang

Ulcerative colitis (UC) is a chronic inflammatory disease with an unclear pathogenesis. This study aimed to investigate the therapeutic mechanism of leonurine in UC. Using network pharmacology and bioinformatics analysis, we identified the PINK1/Parkin-mediated mitophagy pathway as a key target. Validation in a DSS-induced colitis mice model showed that leonurine significantly alleviated colonic injury, reduced inflammatory cytokines, and restored intestinal barrier function. Mechanistically, leonurine upregulated the expression of mitophagy-related proteins (PINK1, Parkin, LC3II) and improved mitochondrial morphology. In conclusion, leonurine ameliorates UC by activating the PINK1/Parkin-mediated mitophagy pathway, providing a scientific basis for its development as a potential therapeutic agent.

溃疡性结肠炎是一种慢性炎症性疾病,其发病机制尚不清楚。本研究旨在探讨leonurine对UC的治疗机制。通过网络药理学和生物信息学分析,我们确定了PINK1/帕金森介导的有丝分裂途径是一个关键靶点。dss诱导的结肠炎小鼠模型验证表明,leonurine可显著减轻结肠损伤,降低炎症因子,恢复肠道屏障功能。机制上,leonurine上调线粒体自噬相关蛋白(PINK1, Parkin, LC3II)的表达,改善线粒体形态。综上所述,leonurine通过激活PINK1/ parkin介导的线粒体自噬途径改善UC,为其作为一种潜在的治疗剂的开发提供了科学依据。
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引用次数: 0
Gambogic acid ameliorates hepatocellular carcinoma by inhibiting oxidative stress via Nrf2-pSmad2C/2L pathway. 藤黄酸通过Nrf2-pSmad2C/2L途径抑制氧化应激,改善肝癌。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-05 DOI: 10.1007/s00210-026-05039-9
Liying Mao, Gaoyang Zhao, Yunyun Zhao, Xinyu Liu, Xiunian Shi, Yingying Xu, Yuqing Chen, Jingqi Zhou, Yihan Li, Yan Yang, Yongfang Gong

Gambogic acid (GA), a natural active ingredient extracted from gamboge resin, has traditionally been utilized for liver-related diseases. Prior investigations have confirmed that GA holds remarkable efficacy in mitigating inflammatory response through the Nrf2 signaling pathway; also, Nrf2 acts synergistically with TGF-β1/Smad2 in hepatocarcinogenesis. However, scientific evidence concerning how GA modulates the TGF-β1/Smad2 and Nrf2/HO-1 signaling pathways and even Nrf2 inhibition on Smad2C/2L phosphorylation relates to the hepatoprotective ability of GA on oxidative stress remains opaque. Nowadays, DEN/CCl4/C2H5OH (DCC) induced HCC in mice, and TGF-β1 and/or Nrf2 inhibitor stimulated HepG2 cells were generated to settle the above questions. As it turns out, GA significantly inhibited the occurrence and progression of liver cancer, as reflected by amelioration in liver biopsies, liver function, and histopathology; while also markedly reducing tumor incidence and multiplicity. It had a notable effect on the activation of Nrf2/AREs-related proteins and inhibition on pSmad2C/2L expression. Cell experiments further confirmed that Nrf2 and pSmad2C/2L may simultaneously participate in the anti-HCC effect of GA, and the Nrf2 inhibitor ML385 could abate GA's anti-HCC effect on proliferation, migration, and invasion, with Nrf2 and pSmad2C/2L expression levels showing a contrary tendency. These studies highlighted that GA may inhibit oxidative stress to ameliorate hepatocellular carcinoma via the Nrf2-pSmad2C/2L pathway. However, the specific interaction regulatory mechanism deserves further exploration.

藤黄酸(GA)是一种从藤黄树脂中提取的天然活性成分,传统上用于肝脏相关疾病。先前的研究证实,GA通过Nrf2信号通路具有显著的减轻炎症反应的功效;Nrf2在肝癌发生中与TGF-β1/Smad2协同作用。然而,关于GA如何调节TGF-β1/Smad2和Nrf2/HO-1信号通路,甚至Nrf2对Smad2C/2L磷酸化的抑制与GA对氧化应激的肝保护能力有关的科学证据尚不清楚。目前,DEN/CCl4/C2H5OH (DCC)诱导小鼠肝癌,生成TGF-β1和/或Nrf2抑制剂刺激HepG2细胞来解决上述问题。结果表明,GA显著抑制肝癌的发生和进展,这反映在肝活检、肝功能和组织病理学的改善上;同时还能显著降低肿瘤的发病率和多样性。对Nrf2/ ares相关蛋白的激活和pSmad2C/2L表达的抑制作用显著。细胞实验进一步证实Nrf2和pSmad2C/2L可能同时参与GA的抗hcc作用,Nrf2抑制剂ML385可减弱GA的抗hcc增殖、迁移和侵袭作用,且Nrf2和pSmad2C/2L表达水平呈相反趋势。这些研究强调,GA可能通过Nrf2-pSmad2C/2L途径抑制氧化应激以改善肝细胞癌。但具体的相互作用调控机制有待进一步探讨。
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引用次数: 0
Enhancing nail disease diagnosis: a capsule network with SE attention and dual backbone models. 增强甲病诊断:具有SE关注和双骨干模型的胶囊网络。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2026-02-04 DOI: 10.1007/s00210-025-04971-6
Arpanpreet Kaur, Rahul Singh, K L Raghavender Reddy, Nabil Elkadhi, Gadug Sudhamsu, Rahul Chauhan, Omar Awad Alsaidan, Sami I Alzarea, Dhaval Mehta, Jigna Prajapati

Nail diseases, including fungal infections and malignancies, pose significant health risks and may lead to severe complications if not accurately diagnosed. Conventional diagnostic methods are often subjective and time-consuming. This study introduces CapsuleSEDualNet, a novel deep learning framework designed to achieve robust and interpretable multi-class nail disease diagnosis. The proposed CapsuleSEDualNet integrates a Capsule Network head with a Squeeze-and-Excitation (SE) attention mechanism within a Dual-Backbone architecture combining MobileNetV2 and DenseNet121. The SE block enhances feature discriminability, while the Capsule head preserves spatial hierarchies for improved interpretability. To address dataset imbalance, the Synthetic Minority Over-sampling Technique (SMOTE) was applied. The model was evaluated using extensive experiments and benchmarked against existing deep learning architectures. CapsuleSEDualNet achieved an overall classification accuracy of 96%, demonstrating superior performance compared to baseline models. The integration of SE attention and Capsule networks effectively reduced misclassification rates and improved feature representation. Experimental findings confirm the framework's robustness, scalability, and interpretability for clinical applications. The proposed CapsuleSEDualNet framework provides an efficient and reliable solution for automated nail disease screening. By combining diagnostic accuracy, model interpretability, and computational efficiency, it addresses a critical clinical need for early and accessible dermatological assessment. The model shows strong potential as a computer-aided decision support tool, pending further clinical validation. Its potential integration into computer-aided dermatology systems and telemedicine platforms can enhance physician decision-making, reduce misdiagnosis risk, and improve patient outcomes in dermatological care.

指甲疾病,包括真菌感染和恶性肿瘤,构成重大健康风险,如果诊断不准确,可能导致严重并发症。传统的诊断方法往往是主观的,耗时的。本研究介绍了一种新的深度学习框架,荚膜edualnet,旨在实现稳健和可解释的多类别指甲疾病诊断。提出的CapsuleSEDualNet在结合MobileNetV2和DenseNet121的双骨干架构中集成了一个带有挤压和激励(SE)注意机制的胶囊网络头。SE块增强了特征的可辨别性,而胶囊头保留了空间层次结构,以提高可解释性。为了解决数据不平衡问题,采用了合成少数派过采样技术(SMOTE)。该模型通过广泛的实验进行评估,并针对现有的深度学习架构进行基准测试。与基线模型相比,CapsuleSEDualNet的总体分类准确率达到96%,表现出优越的性能。SE注意和Capsule网络的集成有效降低了误分类率,改善了特征表示。实验结果证实了该框架在临床应用中的鲁棒性、可扩展性和可解释性。所提出的CapsuleSEDualNet框架为自动指甲疾病筛查提供了高效可靠的解决方案。通过结合诊断准确性,模型可解释性和计算效率,它解决了早期和可访问的皮肤病评估的关键临床需求。该模型显示了作为计算机辅助决策支持工具的强大潜力,有待进一步的临床验证。它与计算机辅助皮肤科系统和远程医疗平台的潜在集成可以增强医生的决策,减少误诊风险,并改善皮肤科护理的患者结果。
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Naunyn-Schmiedeberg's archives of pharmacology
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