Current medicinal chemistry最新文献

{"title":"Identification and Validation of Diagnostic Biomarkers for Osteoarthritis Coexisting with IVDD and LFH via Bioinformatics and Machine Learning.","authors":"Weiqi Han, Zhibo Deng, Zhao Lin, Jun Luo, Jie Xu","doi":"10.2174/0109298673376040250720163154","DOIUrl":"https://doi.org/10.2174/0109298673376040250720163154","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoarthritis (OA), intervertebral disc degeneration (IVDD), and ligamentum flavum hypertrophy (LFH) frequently manifest concurrently in the aging population. This study aims to identify potential diagnostic genes associated with these three interconnected conditions.</p><p><strong>Methods: </strong>Utilizing datasets from the Gene Expression Omnibus (GEO) database, we applied Limma and weighted gene co-expression network analysis (WGCNA) to discern pivotal genes. Subsequent enrichment analyses shed light on the functional implications of these identified genes. The utilization of three distinct machine learning algorithms facilitated the identification of hub genes. Evaluation of the predictive capacity of these hub genes was conducted through nomograms and receiver operating characteristic (ROC) curves. Additionally, predictions pertaining to transcription factors, microRNAs, and potential therapeutic drugs were made. Furthermore, the study delved into the exploration of immune cell infiltration in OA.</p><p><strong>Results: </strong>An integrated bioinformatics analysis of OA datasets identified 246 key genes enriched in inflammatory pathways, including MAPK signaling and interleukin signaling. Comparison across OA, IVDD, and LFH datasets identified 9 common differentially expressed genes. Machine learning algorithms subsequently identified ANKH and GADD45B as central hub genes. A diagnostic nomogram constructed using these genes demonstrated strong predictive performance, particularly for OA. Further analyses predicted SREBF1 as a potential co-regulator and quercetin as a drug candidate targeting both hub genes. Immune infiltration analysis revealed altered levels of resting memory CD4 T cells and activated mast cells in OA, correlating with hub gene expression. Finally, RT-qPCR validation in clinical samples confirmed the differential expression patterns of ANKH and GADD45B, supporting their relevance.</p><p><strong>Discussion: </strong>The identification of ANKH and GADD45B as common hub genes offers novel insights into the shared molecular mechanisms underlying co-occurring OA, IVDD, and LFH. The strong predictive performance of the nomogram using these genes underscores their potential as diagnostic biomarkers for OA. The predicted interaction of quercetin with both hub genes, alongside SREBF1 as a co-regulator, suggests new therapeutic targets for these genes. Moreover, the findings on altered activated mast cell levels in OA correlating with hub gene expression highlight their potential role in OA pathogenesis and as therapeutic targets. These findings, supported by initial RT-qPCR validation, provide a foundation for further experimental studies to confirm their clinical utility.</p><p><strong>Conclusion: </strong>This study identifies ANKH and GADD45B as promising diagnostic genes for distinguishing OA co-occurring with IVDD and LFH. Furthermore, our findings underscore the significance of MCs in the","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834912","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":"Identification of PPIA, DPP4, and ITK as Potential Targets of Pterostilbene in Abdominal Aortic Aneurysm: A Network Pharmacology and Molecular Docking Study.","authors":"Weiqi Li, Xiaoyong Xiao, Jing Yang, Dehong Liu, Zhanpeng Sun","doi":"10.2174/0109298673474897260422055145","DOIUrl":"https://doi.org/10.2174/0109298673474897260422055145","url":null,"abstract":"<p><strong>Background: </strong>Pterostilbene is a polyphenolic compound with antioxidant and anti-inflammatory properties. This study aims to explore its potential therapeutic effects on Abdominal Aortic Aneurysm (AAA).</p><p><strong>Methods: </strong>The Gene Expression Omnibus (GEO) database was accessed to obtain single- cell sequencing data and transcriptome datasets to identify Differentially Expressed Genes (DEGs) in AAA. The DEGs were further intersected with predicted targets of pterostilbene to identify common genes, which were considered core genes for functional enrichment analysis and Gene Set Enrichment Analysis (GSEA). Molecular docking and 100 ns Molecular Dynamics (MD) simulations were then performed to evaluate binding affinity and stability.</p><p><strong>Results: </strong>PPIA, DPP4, and ITK were identified as overlapping genes associated with both pterostilbene and AAA. A single-cell atlas revealed their specific expression patterns across different cell types. The three genes were also correlated with IL6/JAK/STAT3, inflammatory response, and immune-related pathways. Molecular docking showed binding affinities ranging from -5.66 to -7.11 kcal/mol, and 100 ns MD simulations revealed stable binding conformations for all three targets.</p><p><strong>Discussion: </strong>The present multi-omics analysis suggests that pterostilbene may exert therapeutic effects on AAA by modulating inflammation- and immune-related pathways, providing a hypothesis-generating basis for further investigation.</p><p><strong>Conclusion: </strong>This hypothesis-generating study proposes that pterostilbene may exert therapeutic effects on AAA by targeting PPIA, DPP4, and ITK and modulating inflammation- and immune-related pathways. However, these computational findings require further experimental validation.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835030","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":"Quantum Consciousness: A Molecular Perspective Involving Glycoprotein-Tunnelling Hypothesis (GPTH).","authors":"Atta-Ur-Rahman","doi":"10.2174/0109298673484734260413095934","DOIUrl":"https://doi.org/10.2174/0109298673484734260413095934","url":null,"abstract":"<p><p>Long-term memory exhibits a remarkable problem: it is extraordinarily stable over decades, yet it supports rapid, flexible cognition, logic, and conscious awareness. Classical neuroscience has largely attributed memory to synaptic plasticity and networklevel dynamics; however, these mechanisms alone do not adequately explain the molecular durability of memory traces in the face of continuous protein turnover. A hypothesis advanced by the author proposes that memory is encoded in stable, folded glycoprotein patterns, particularly within synaptic and peri-synaptic environments. This review examines how such structurally persistent molecular architectures could support dynamic information processing through quantum-enabled chemical mechanisms. Considering recent advances in glycobiology, enzymology, quantum biology, and medicinal chemistry, it is suggested that proton and electron tunnelling provide a plausible and experimentally grounded mechanism for reading out stable glycoprotein-encoded information without requiring large-scale molecular rearrangement or long-lived macroscopic quantum coherence. Such an approach reconciles molecular stability with cognitive flexibility and yields testable predictions that are relevant to neurodegenerative disease and drug discovery.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834458","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":"Antimalarial Effects of Dobinin K against Chloroquine-resistant Plasmodium falciparum Through Disruption of the Parasite's Redox System.","authors":"Long-Fei He, He Sun, Li-Qi Cang, Jin-Da Wang, Chao-Jiang Xiao, Bei Jiang, Lei Shen","doi":"10.2174/0109298673437440260305081236","DOIUrl":"https://doi.org/10.2174/0109298673437440260305081236","url":null,"abstract":"<p><strong>Objective: </strong>The current study was designed to systematically evaluate the antiplasmodial ability of Dobinin K against the chloroquine-resistant strain of Plasmodium falciparum (P. falciparum) Dd2 and investigate its potential mechanism of action.</p><p><strong>Methods: </strong>The effects of Dobinin K against Dd2 were assessed by both SYBR Green I fluorescence assay and Giemsa staining assay. Transcriptomic analysis was performed to examine global gene expression changes in P. falciparum following Dobinin K treatment. To explore the acting mechanism of Dobinin K on Dd2, contents of redox substrates and metabolites, as well as the activities of enzymes, were examined using the corresponding kit. Ultrastructural analysis was performed using transmission electron microscopy. The mitochondrial membrane potential (ΔΨm) was assessed based on JC-1 fluorescence intensity. The mRNA expression levels were analyzed through qRT-PCR. DNA fragmentation during apoptosis was evaluated using the TUNEL assay.</p><p><strong>Results: </strong>Dobinin K exhibited antiplasmodial activity against Dd2 that was both concentration- and time-dependent, affecting all developmental stages of the parasite. Transcriptomic analysis suggested that the mechanism of action of Dobinin K refers to the disruption of the redox system in the parasite. Dobinin K increased the levels of oxidative products, elevated the GSSG / GSH ratio, inhibited the activities of antioxidant enzymes, including PfGR, PfTrxR, and PfSOD, decreased the NADP+ / NADPH ratio, disruptedΔΨm, upregulated mRNA expression of most essential apicoplast metabolic enzymes, and ultimately induced apoptosis in Dd2.</p><p><strong>Discussion: </strong>Artemisinin-based combination therapies for chloroquine-resistant malaria face tremendous challenges due to the occurrence of artemisinin resistance. Our findings suggested that Dobinin K exerted its antimalarial effects by disrupting the parasite's redox homeostasis, a mechanism that differs from artemisinin. This further supports redox system targeting as an effective strategy against chloroquine-resistant P. falciparum.</p><p><strong>Conclusion: </strong>Dobinin K disrupts the redox system of P. falciparum, subsequently disturbing mitochondrial and apicoplast functions and triggering apoptosis in Dd2.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834935","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":"Identifying Key Pathogenic Mechanisms in Recurrent Glioblastoma Through Bioinformatics Analysis.","authors":"Xuan Rong, Mingyang Han, Luhao Bao, Zihao Wang, Valentin Pavlov, Ilgiz Gareev, Jianing Wu, Xingli Dong","doi":"10.2174/0109298673405762251209135005","DOIUrl":"https://doi.org/10.2174/0109298673405762251209135005","url":null,"abstract":"<p><strong>Introduction: </strong>Despite aggressive surgery and adjuvant therapy, glioblastoma commonly recurs within months. We aimed to identify key genes and microRNAs (miRNAs)- mRNA regulatory networks associated with recurrent glioblastoma and to nominate candidate repurposable drugs.</p><p><strong>Methods: </strong>Two mRNA expression datasets (GSE58399 and GSE42669) from GEO were analyzed to identify differentially expressed genes (DEGs) between recurrent and primary tumors. Functional enrichment (Gene Ontology, KEGG) characterized implicated processes and pathways. A protein-protein interaction network (STRING and Cytoscape) identified hub genes. miRWalk 3.0, integrating TargetScan, miRDB, and miRTarBase, predicted miRNAs targeting hub genes and defined miRNA-mRNA interactions. The Connectivity Map (CMap) was used to prioritize small molecules predicted to reverse the DEGs signature. Kaplan-Meier survival analyses assessed associations between candidate genes and patient outcomes.</p><p><strong>Results: </strong>We identified 201 DEGs and constructed a PPI network comprising 180 nodes and 337 edges. Ten hub genes were prioritized. CMap nominated five top candidate compounds- levamisole, chlorzoxazone, ranitidine, atovaquone, and chrysin-as potential therapeutics for glioblastoma recurrence. Synaptotagmin 1 (SYT1) emerged among hub genes and was predicted to be regulated by 12 miRNAs. Elevated SYT1 expression correlated with poorer overall and progression-free survival in recurrent glioblastoma patients.</p><p><strong>Discussion: </strong>This integrative analysis highlights SYT1 and its upstream miRNAs as candidate biomarkers and potential therapeutic targets in recurrent glioblastoma and proposes several repurposable compounds for experimental validation. Further functional studies and clinical validation are required prior to translation.</p><p><strong>Conclusion: </strong>Collectively, this study offers valuable insights into the regulatory landscape of recurrent glioblastoma and lays the groundwork for more targeted and personalized therapeutic approaches.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834960","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":"Prognostic and Immunoinfiltration Analysis of Transcription Factor BTF3 in Pan-cancer.","authors":"Xiaoxiao Liu, Xiaolan Zhang, Ruixue Sun, Hongyang Du","doi":"10.2174/0109298673383163251013124752","DOIUrl":"https://doi.org/10.2174/0109298673383163251013124752","url":null,"abstract":"<p><strong>Introduction: </strong>BTF3, also known as BETA-NAC, BTF3b, BTF3a, and NACB, is a transcription factor originally isolated from HeLa cell extracts. It forms stable complexes with RNA polymerase II and plays a critical role in transcription initiation. Although aberrant BTF3 expression has been reported in certain malignancies, its overall role across diverse tumor types remains poorly defined. This study aimed to elucidate the functional implications of BTF3 across various cancers.</p><p><strong>Methods: </strong>BTF3 expression was analyzed using datasets from The Cancer Genome Atlas (TCGA), including TCGA_GTEx, TCGA unpaired, and TCGA paired samples. The prognostic significance of BTF3 across 33 tumor types was evaluated using Kaplan-Meier survival and univariate Cox regression analyses. In cancers where BTF3 expression showed prognostic value, additional clinical correlation analyses were performed. Clear cell renal carcinoma (sample size >500) was selected for nomogram construction to illustrate BTF3's prognostic relevance. The association between BTF3 expression and immune cell infiltration was also examined, alongside functional enrichment analysis to explore involved signaling pathways.</p><p><strong>Results: </strong>BTF3 displayed variable expression across tumor types and was significantly correlated with several clinical parameters. Survival and regression analyses identified BTF3 as a prognostic marker in specific cancers. The nomogram model for clear cell renal carcinoma further supported its predictive value. BTF3 expression was also associated with features of the tumor immune microenvironment. Functional enrichment analysis implicated signaling pathways, including the tuberous sclerosis complex/mechanistic target of rapamycin (TSC/mTOR), phosphoinositide 3-kinase/AKT (PI3K/AKT), and rat sarcoma/mitogen-activated protein kinase (RAS/MAPK) in BTF3-associated tumorigenesis.</p><p><strong>Discussion: </strong>These findings underscore the heterogeneous expression of BTF3 across malignancies and highlight its potential involvement in modulating the tumor immune landscape and oncogenic signaling pathways. The results expand our understanding of BTF3's role in cancer biology and suggest mechanistic links to well-characterized tumorigenic processes. However, further experimental validation is necessary to substantiate these associations.</p><p><strong>Conclusion: </strong>BTF3 may serve as a promising prognostic biomarker and a potential target for immunotherapeutic intervention across multiple cancer types.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834198","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":"Research Trends and Future Prospects on Solid Lipid Nanoparticles in the Early 21st Century - A Bibliometric Analysis.","authors":"Qirui Hu, Fanyu Meng, Shuping Jia, Yizhou Wang, Xiaoying Jin, Danni Wang, Zhongqing Wang","doi":"10.2174/0109298673447840260114055416","DOIUrl":"https://doi.org/10.2174/0109298673447840260114055416","url":null,"abstract":"<p><strong>Background: </strong>Research on Solid Lipid Nanoparticles has increased significantly due to their ability to improve drug delivery and control drug release from lipids. This bibliometric study illustrated SLN's evolution, co-authored networks between researchers, and research trends.</p><p><strong>Methods: </strong>We analyzed 5,063 'Article' type publications obtained from the Web of Science Core Collection using the multi-tools VOSviewer, CiteSpace, and HistCite.</p><p><strong>Results: </strong>Solid Lipid Nanoparticles' journal growth for publications and citations highlighted continued scientific interest in this area. India was the most productive country (1,003 publications). At the same time, the Free University of Berlin was the most productive institution, and the most productive authors, Souto, Eliana B. (98 publications, 16 collaborative links), and Mueller, R.H. (82 publications, 7 collaborative links), formed the core of the co-authorship network. Keywords associated and emerging frontiers indicated an innovative field evolving from formulation studies to one focused on application data.</p><p><strong>Discussion: </strong>We traced the trajectory from the lowest-hanging fruit to use cases in grand challenges, but coverage of database bias remains a concern.</p><p><strong>Conclusion: </strong>The past twenty years have witnessed an increase in publications and citations, as evidenced by active contributions from numerous countries, institutions, and authors. Keyword analysis and emerging frontiers marked their hot topics and research directions.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834499","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":"Antiviral Potential of 3,4-Dimethoxychalcone Against SARS-CoV-2: A Promising Candidate.","authors":"Washington Kleber Rodrigues Lima, Glaucio Monteiro Ferreira, Claudia Zeneida Gomes Parente Alves Lima, Eduardo Willian de Alencar Pereira, Livia Mendonça Munhoz Dati, Vitor Galvão Lopes, Víctor Kleber Gomes Parente Alves Lima, Layana Sousa Ferreira, Cláudia Quintino da Rocha, Rodrigo Portes Ureshino, Robertha Lemes, Roberta Sessa Stilhano, Tiago Nicoliche, Carla Máximo Prado, Liria Hiromi Okuda, Kennedy Bonjour, Mario Hiroyuki Hirata, Lidio Gonçalves Lima-Neto","doi":"10.2174/0109298673388849260203095838","DOIUrl":"https://doi.org/10.2174/0109298673388849260203095838","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to investigate the potential of LQPN-05, a compound derived from Fridericia platyphylla flowers, as a novel antiviral agent against SARS-CoV-2.</p><p><strong>Methods: </strong>Molecular modeling and dynamics simulations were used to analyze the interaction between LQPN-05 and the SARS-CoV-2 spike protein. In vitro assays assessed spike protein thermal stability and antiviral activity in infected cells. Cytotoxicity was evaluated in cell lines, and efficacy was further tested in an animal model of SARS-CoV- -2 infection.</p><p><strong>Results: </strong>Simulations revealed favorable binding of LQPN-05 to the spike protein, particularly protomer C. In vitro, LQPN-05 modified the spike protein's melting temperature and inhibited viral replication. The compound showed minimal cytotoxicity and, in vivo, helped maintain animal weight and cellular lung organization per fractal analysis.</p><p><strong>Discussion: </strong>The results signify LQPN-05's potential as a spike protein inhibitor from a natural source. Its efficacy amid concerns of drug resistance is notable. Study limitations include the preliminary nature of the in vivo findings.</p><p><strong>Conclusion: </strong>LQPN-05 demonstrates promising anti-SARS-CoV-2 activity, underscoring the value of exploring natural compounds for antiviral therapy against emerging pathogens.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834911","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":"Studies on Oxidative Stability of Vegetable Oil During Frying.","authors":"Antara Roy, Dilip K Maiti, Bimal Krishna Banik","doi":"10.2174/0109298673420768251118055905","DOIUrl":"https://doi.org/10.2174/0109298673420768251118055905","url":null,"abstract":"<p><strong>Background: </strong>To study various reactions during frying with vegetable oil is an interesting topic because people have been using this process daily. Despite the widespread daily use of deep frying, the high temperatures involved lead to chemical degradation of vegetable oils, including hydrolysis, oxidation, and polymerization, which not only reduce their oxidative stability but also diminish nutritional quality and may generate harmful compounds such as 4-HNE. While antioxidant additives and oil blending are potential strategies to mitigate these effects, limited research exists on how specific blends of mustard and sesame oil, with added antioxidants, perform under high-temperature frying conditions. This study addresses this gap by systematically evaluating the oxidative stability of such a blend during deep frying, using multiple chemical indices to track degradation.</p><p><strong>Objective: </strong>This study focused on various chemical measures to assess the degradation and oxidation of the oil (a combination of sesame and mustard oil with additional antioxidants), including 4-HNE value, conjugated diene, peroxide value, para-anisidine value, acid value, iodine value, and conjugated triene values. An experimental model is created to evaluate the oxidative stability of mustard and sesame oil when fried at high temperatures.</p><p><strong>Methods: </strong>Peeled potatoes are deep-fried with blended oil, and numerous chemical reactions are followed during this process.</p><p><strong>Results: </strong>Vegetable oil undergoes hydrolysis, oxidation, and polymerization during deep frying, which reduces its oxidative stability and causes a decline in its nutritional benefits. Blending prevents oxidation in oil.</p><p><strong>Discussion: </strong>Blending prevents oxidation in oil as well as prevents hydrolysis, oxidation, and polymerization during deep frying, and thus it protects oxidative stability and nutritional benefits.</p><p><strong>Conclusion: </strong>Oils undergo a number of reactions during deep-frying, including hydrolysis, catalytic oxidation, and thermal alteration. These processes produce a variety of compounds, some of which create health problems. But blended oil prevents oxidation than single-use oil.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834512","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":"Ginsenoside Re Suppresses Tumorigenesis in NSCLC through PERKMediated Endoplasmic Reticulum Stress and the Mitochondrial Apoptosis Pathway.","authors":"Jiaqi Zhao, Xinze Liu, Kaijing Sun, Renbo Tan, Zhengwu Liu, Shuang Zu, Anning Li, Lin Feng, Guangzhe Li, Changbao Chen, Xin Jin, Xilin Wan","doi":"10.2174/0109298673422496260121045046","DOIUrl":"https://doi.org/10.2174/0109298673422496260121045046","url":null,"abstract":"<p><strong>Introduction: </strong>To investigate the antitumor effects of ginsenoside Re on human non-small cell lung cancer cells, specifically the NCI-H460 and 95D cell lines.</p><p><strong>Methods: </strong>This study investigated the effects of ginsenoside Re on the proliferation of two cell lines using the CCK-8 assay; observed changes in cell morphology using DAPI and AO/EB staining; analyzed cell cycle and apoptosis rate using flow cytometry; and evaluated cell migration and invasion ability using Transwell and wound healing assays. Western blotting and qPCR results indicated that ginsenoside Re induces apoptosis in NCI-H460 and 95D cells by regulating the expression of genes and proteins, including Bax, BIP, CHOP, eIF-2α, Bcl-2, and β-actin.</p><p><strong>Results: </strong>Ginsenoside Re inhibited the proliferation of two cell types in a time- and dosedependent manner. Cell cycle analysis revealed that ginsenoside Re induced G2 phase arrest in NCI-H460 cells and G1/S phase arrest in 95D cells, and that the morphology of apoptosis could be visualized by DAPI and AO/EB fluorescence staining. Cell scratchhealing and invasion assays confirmed that ginsenoside Re inhibited the invasion and migration of NCI-H460 and 95D cells, and the coverage of 95D cells decreased from 73.17±0.26% to 33.02±0.40%.</p><p><strong>Discussion: </strong>Ginsenoside Re significantly inhibited NSCLC 95D and NCI-H460 cells by suppressing proliferation, cell cycle progression, migration, invasion, and inducing apoptosis.</p><p><strong>Conclusion: </strong>Ginsenoside Re can effectively induce tumor cell apoptosis by regulating the endoplasmic reticulum apoptosis pathway and thereby exert anti-tumor effects. The experiment provides a reliable basis for establishing a mechanistic framework explaining the role of ginsenoside Re in non-small cell lung cancer.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834946","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}