Journal of pharmaceutical analysis最新文献

{"title":"Unraveling the mechanism of Lianqiaobaidu powder in viral myocarditis: Complementary actions within cardiac cell types.","authors":"Na Tang, Shuqiao Xing, Ting Zhou, Wen-Hui Qi, Bingyan Wang, Chengwen Li, Wei Cao, Zhi-Jing Zhao, Yingfeng Lei, Xiao-Qiang Li","doi":"10.1016/j.jpha.2026.101595","DOIUrl":"https://doi.org/10.1016/j.jpha.2026.101595","url":null,"abstract":"<p><p>Image 1.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101595"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13486344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148804398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A facile antibody-mediated CMC platform for targeted screening of CCR1 ligands from <i>Magnolia officinalis</i>.","authors":"Ting Zhang, Shengjie You, Wenhao Chen, Hao Liu, Taiping He, Qiao Zhang, Xiaojuan Tian, Xiang Sun, Limei Liang, Suleixin Yang, Sanyin Zhang, Huachao Bin, Shilin Chen","doi":"10.1016/j.jpha.2026.101699","DOIUrl":"10.1016/j.jpha.2026.101699","url":null,"abstract":"","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101699"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13452308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148698638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advanced analytical approaches for endocannabinoids and endocannabinoid-like substances: Applications in liver disease research.","authors":"Jun-Yi Zhou, Yan-Qing Chen, Hai-Yu Zhao, Jian-Bo Wan","doi":"10.1016/j.jpha.2026.101546","DOIUrl":"https://doi.org/10.1016/j.jpha.2026.101546","url":null,"abstract":"<p><p>Endocannabinoids (eCBs) and eCB-like substances are lipid mediators that play vital roles in regulating diverse physiological and pathological processes. These effects are predominantly mediated through interactions with cannabinoid receptors (CBRs), particularly CB1R and CB2R. Due to their typically low abundance in biological samples, the development of precise and efficient analytical methods is essential for accurate quantification of eCBs. The liver serves as a critical site of eCB activity, where dysregulation of eCB levels has been associated with various liver diseases. This review focuses on recent advancements in sample preparation and analytical techniques for eCBs and eCB-like substances from 2017 to 2024, providing a comprehensive evaluation of their strengths and limitations. Additionally, the roles of eCBs in liver lipid metabolism and their involvement in pathological processes are explored in detail. eCBs and eCB-like substances hold promise as diagnostic biomarkers, offering significant potential for applications in both basic research and clinical practice.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101546"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13476560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148763976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of lotus seeds stored over different periods by analyzing the changes in the chemical structure of starch.","authors":"Xi-Jun Lian, Ruo-Meng Zhang, Yu-Jia Shen, Xue-Xiao Cao, Qiu-Ping Wei, Chang-Jiang-Sheng Lai","doi":"10.1016/j.jpha.2026.101594","DOIUrl":"https://doi.org/10.1016/j.jpha.2026.101594","url":null,"abstract":"<p><p>Image 1.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101594"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13485638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148804369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arctigenin discovered by high-throughput screening ameliorates doxorubicin-induced cardiotoxicity as a novel natural KEAP1-NRF2 inhibitor.","authors":"Xinyu Heng, Chao Ye, Shaohong Huang, Ke Zhang, Yankui Liu, Yueyue Wu, Ning Sun, Hai Yang","doi":"10.1016/j.jpha.2026.101606","DOIUrl":"https://doi.org/10.1016/j.jpha.2026.101606","url":null,"abstract":"<p><p>Doxorubicin (DOX), a widely used chemotherapeutic, is significantly limited by dose-dependent cardiotoxicity characterized by oxidative stress, mitochondrial dysfunction, and ferroptosis. Despite decades of research, dexrazoxane (DXZ) remains the only approved cardioprotectant, yet its clinical utility is constrained by potential reduction in efficacy and systemic toxicity. Effective alternatives are therefore urgently needed. Through high-throughput screening of a 960-compound natural product library, we identified arctigenin (ATG), a major bioactive compound from the Asian medicinal plant <i>Arctium lappa</i> L., as a promising cardioprotective candidate against DOX-induced cardiotoxicity (DIC). Both <i>in vitro</i> and <i>in vivo</i> studies demonstrated that ATG significantly attenuated DOX-induced cell death, reduced reactive oxygen species (ROS) accumulation, inhibited ferroptosis, preserved mitochondrial function, and improved cardiac function and myocardial structural integrity in mice. Mechanistically, ATG activated the nuclear factor erythroid 2-related factor 2 (NRF2)-antioxidant response element (ARE) pathway by binding to the serine 602 (S602) residue of Kelch-like ECH-associated protein 1 (KEAP1), which competitively inhibited the KEAP1-NRF2 interaction. This binding facilitated the dissociation of NRF2 from KEAP1, resulting in reduced NRF2 ubiquitination, increased nuclear accumulation of NRF2, and enhanced transcription of downstream target genes. Collectively, our results identify ATG as a novel NRF2 activator that alleviates DIC through suppression oxidative stress and ferroptosis by directly targeting the KEAP1-NRF2-ARE axis.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101606"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13475220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148762961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Probucol inhibits palmitic acid-mediated renal calcium oxalate stone formation by targeting KLF5-PPARγ axis-mediated lipotoxicity.","authors":"Haotian Ren, Yutong Chen, Yang Li, Jingdong Zhang, Yi Shao, Bangxian Yu, Linguo Xie, Shiyong Qi, Rui Wang, Zhiqun Shang, Chunyu Liu","doi":"10.1016/j.jpha.2026.101575","DOIUrl":"10.1016/j.jpha.2026.101575","url":null,"abstract":"<p><p>The pathogenesis of renal calcium oxalate (CaOx) stone is multifaceted and closely associated with metabolic disturbances. Palmitic acid (PA), a major saturated fatty acid, has emerged as a key contributor to CaOx stone formation. In this study, high-throughput drug screening identified probucol as a potential therapeutic agent capable of alleviating PA-mediated renal CaOx crystal formation <i>in vitro</i> and <i>in vivo</i>. Mechanistically, PA upregulates Krüppel-like factor 5 (KLF5), which transcriptionally activates peroxisome proliferator activated receptor gamma (PPARγ) and thereby drives lipotoxicity. Probucol directly binds to arginine-440 (Arg440) within the zinc finger DNA-binding domain of KLF5, competitively inhibiting its DNA-binding ability. This inhibition suppresses PPARγ expression and mitigates PPARγ-mediated lipotoxicity. Collectively, our findings identify KLF5 as a novel intracellular target of probucol, and highlight its therapeutic potential in treating PA-mediated renal CaOx stone formation by mitigating lipotoxicity.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101575"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13495608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148804364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PKM2: A gatekeeper in macrophage metabolic reprogramming.","authors":"Ke Li, Mingyu Wu, Qiuyu Zhang, Jiabin Wu, Xianyi Ding, Weihua Xiao","doi":"10.1016/j.jpha.2026.101564","DOIUrl":"https://doi.org/10.1016/j.jpha.2026.101564","url":null,"abstract":"<p><p>Metabolic reprogramming serves as a core adaptive mechanism for cells to respond to microenvironmental changes and plays a decisive role in macrophage functional polarization. Pyruvate kinase M2 (PKM2), recognized for its dynamic allosteric regulation, acts as a critical molecular hub linking metabolic reprogramming with immune responses. Despite numerous studies affirming the pivotal role of PKM2 in tumor metabolism, its complex regulatory mechanisms within the immune metabolic network remain inadequately defined, significantly hindering the advancement of targeted therapeutic strategies for metabolic reprogramming. This review meticulously analyzes and highlights the significance of PKM2-mediated metabolic reprogramming in macrophages across several organ disorders. We subsequently examined various PKM2 inhibitors and activators, along with natural compounds that modulate PKM2, as research evidence for therapeutic approaches to diseases, particularly with the metabolic reprogramming of macrophages. This study comprehensively examines the theoretical foundation, research evidence, and intervention strategies regarding PKM2 as a crucial regulatory element of macrophages, offering novel perspectives on therapeutic approaches for macrophage metabolic reprogramming.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101564"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13485507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148804389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut-brain axis dysregulation in Parkinson's disease: Mechanisms linking microbiota to neuroinflammation and α-synuclein pathology.","authors":"Zhenxiong Zhao, Mengdie Dong, Zhen Mu, Zhencang Zheng, Zhengwei Zhang","doi":"10.1016/j.jpha.2025.101521","DOIUrl":"https://doi.org/10.1016/j.jpha.2025.101521","url":null,"abstract":"<p><p>Parkinson's disease (PD) is increasingly understood as a multisystem disorder originating not only in the central nervous system (CNS) but also involving the gut-brain axis (GBA). A key driver of PD pathogenesis is gut microbiota dysbiosis, which contributes to disease progression by inducing intestinal inflammation, altered microbial metabolite production, and compromised gut barrier integrity. These alterations can initiate the misfolding and aggregation of α-synuclein in the enteric nervous system (ENS), facilitating its spread to the CNS via vagal pathways. Furthermore, microbiota-derived molecules, including short-chain fatty acids (SCFAs) and lipopolysaccharides (LPS), are implicated in triggering systemic and neuroinflammatory cascades that exacerbate the degeneration of dopaminergic neurons. This review consolidates current evidence on the mechanistic connections between gut microbiota dysregulation, neuroinflammation, and α-synuclein pathology in PD. We also discuss the translational potential of microbiota-focused biomarkers and innovative therapeutic strategies, providing new perspectives for early diagnosis and disease modification. Elucidating the GBA in PD paves the way for personalized medicine and microbiome-targeted therapies.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101521"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13470196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148764098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diosgenin presents a novel role in promoting diabetic wound healing: A mechanism involving Sirt6/Nrf2-mediated inhibition of ferroptosis.","authors":"Ji-Qi Wang, Lu Chen, Yu-Zhe Lin, Xiu-Zhi Zhang, Yi-Tian Yu, Yi-Han Lin, Li-Jiang Han, Yi-Yun Lv, Nai-Feng Tian, Zhen Lin, Wei-Jun Guo","doi":"10.1016/j.jpha.2026.101635","DOIUrl":"https://doi.org/10.1016/j.jpha.2026.101635","url":null,"abstract":"<p><p>Delayed wound healing in patients with diabetes is frequently caused by the dysfunction of human umbilical vein endothelial cells (HUVECs). Under high-glucose and high-fat (HGHF) conditions, the microenvironment induces uncontrolled lipid peroxidation and subsequent iron-dependent ferroptosis. Diosgenin (DG), a steroidal saponin extracted from herbs, including wild yam, exhibits diverse pharmacological activities. The present study aimed to investigate the role and underlying mechanism of DG in HGHF-induced ferroptosis and diabetic wound (DW) healing. A DW model was established in mice by intraperitoneal injection of streptozotocin (STZ). HUVECs were cultured under HGHF conditions to induce the diabetic microenvironment. C11-BODIPY, FerroOrange probes, and hematoxylin-eosin (H&E)/Masson staining were used to determine lipid peroxidation, iron ion levels, and histological changes, respectively. Results demonstrated that DG alleviated HGHF-induced ferroptosis, as evidenced by reduced malondialdehyde (MDA), lipid peroxidation, and mitochondrial reactive oxygen species (ROS) levels, and increased glutathione (GSH) levels. Additionally, DG upregulated the expression of the anti-ferroptotic protein glutathione peroxidase 4 (GPX4), promoted angiogenesis, and accelerated wound healing in diabetic mice. Network pharmacology analysis identified the sirtuin 6/nuclear factor erythroid 2-related factor 2 (Sirt6/Nrf2) pathway as a potential target of DG, a finding validated by mechanistic studies. Silencing Sirt6 in HUVECs negated the protective effect of DG against ferroptosis. In conclusion, DG mitigates ferroptosis and promotes DW healing, at least partially through activating the Sirt6/Nrf2 pathway.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101635"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13486993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148804270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating mass spectrometry imaging and data-driven segmentation for spatial metabolic mapping of diabetic eye disease.","authors":"Shuohan Cheng, Shuo Wang, Tianfang Lan, Hongtao Jin, Zhi Zhou, Zhonghua Wang, Zeper Abliz","doi":"10.1016/j.jpha.2026.101596","DOIUrl":"https://doi.org/10.1016/j.jpha.2026.101596","url":null,"abstract":"<p><p>Diabetic eye disease (DED) is a leading cause of vision impairment worldwide, yet the molecular mechanisms underlying its progression remain incompletely understood. In this study, we applied a dual-platform spatial metabolomics strategy integrating air flow-assisted desorption electrospray ionization mass spectrometry imaging (AFADESI-MSI) and matrix-assisted laser desorption ionization mass spectrometry imaging (MALDI-MSI) to characterize spatial metabolic alterations in the eyes of diabetic rats. Data-driven segmentation of retinal micro-regions using SCiLS Lab software enabled fine-scale mapping of metabolic heterogeneity. Physiological, biochemical, and histopathological analyses were combined with spatial metabolite mapping to construct a metabolic atlas and evaluate the regulatory effects of ferulic acid. We established a comprehensive spatial metabolome atlas of the rat eye, identifying 135 annotated metabolites and revealing significant region-specific metabolic heterogeneity. Unsupervised k-means clustering was further applied to the high-resolution MALDI-MSI data, successfully delineating distinct functional micro-regions of the retina solely based on endogenous metabolic profiles, demonstrating the power of data-driven tissue segmentation. In diabetic eyes, 39 metabolites were significantly dysregulated, involving amino acid, glucose, lipid, and redox metabolism. Notably, lysine, arginine, carnitine, and glutathione (GSH) were depleted, while glucose-6-phosphate (G6P), glycerol-3-phosphate (G3P), and pro-inflammatory lipids were elevated, highlighting profound metabolic reprogramming across ocular compartments. Ferulic acid treatment restored nine key metabolites, alleviated oxidative stress, normalized lipid and glucose metabolism, and improved retinal structural integrity in a dose-dependent manner. This study shows that integrating mass spectrometry imaging with data-driven tissue segmentation reveals spatial metabolic reprogramming in DED and highlights ferulic acid as a promising therapeutic candidate.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"16 8","pages":"101596"},"PeriodicalIF":8.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13486337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148804366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}