Combinatorial chemistry & high throughput screening最新文献

{"title":"Investigation of the Potential Pharmacological Substance Basis and Mechanism of Action of Xuantu Granules in Treating Diabetic Kidney Disease Based on UHPLC-Q-Exactive-HRMS and Bioinformatics.","authors":"Jingna Fan, Chang Kong, Bin Yu, Rong Wang, Zhenqiang Qi","doi":"10.2174/0113862073364424241202111833","DOIUrl":"https://doi.org/10.2174/0113862073364424241202111833","url":null,"abstract":"<p><strong>Objective: </strong>The objective of this study is to analyze and identify the main chemical components and blood-absorbed components of Xuantu Granules and predict their pharmacological substance basis and mechanism in the treatment of DKD.</p><p><strong>Methods: </strong>A DKD rat model was established by feeding SD rats a high-fat and high-sugar diet and administering intraperitoneal injections of streptozotocin (STZ). The therapeutic effect of Xuantu granules was evaluated. Drug-containing serum was prepared after gavage, and the major chemical components of Xuantu Granules and the drug-containing serum were detected using UHPLC-Q-Exactive-HRMS. Blood-absorbed components were identified based on retention time, mass-to-charge ratio, and MS/MS spectrum. Blood-absorbed components' target proteins were searched using the CTD, SwissTarget, BindingDB, and TargetNet databases. DKD disease target genes were screened from the GEO database using WGCNA. A \"bioactive blood-absorbed component-target-disease\" PPI network was constructed using Cytoscape software, and the key clustering subnetworks were identified by MCODE plugin. GO functional analysis and KEGG pathway enrichment analysis were performed on subnetworks.</p><p><strong>Results: </strong>Xuantu Granules lowered fasting blood glucose, improved renal function, reduced proteinuria, and improved renal tissue pathological changes in DKD rats. 36 chemical components were identified, among which 12 compounds, including β -Carboline-1-propionic acid, Morin, Afzelin, Schizandrin, Gomisin A were identified as blood-absorbed components. Bioinformatics analysis indicated that AKT1, TNF, TP53, IL6, SRC, IL1B, EGFR, JUN, BCL2, and CASP3 might be the main therapeutic targets. The involved pathways included the IL-17 signaling pathway, PI3K-Akt signaling pathway, AGE-RAGE signaling pathway in diabetic complications and so on.</p><p><strong>Conclusion: </strong>Xuantu Granules may exert therapeutic effects on DKD through multiple targets and pathways.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945246","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":"Unveiling the Interplay between Dopamine-like Molecules and Β-Amyloid Peptide: A Combined Molecular Dynamic and DFT Approach.","authors":"Mohammad Erfan Zand, Mohammad Reza Bozorgmehr, Mohammad Momen Heravi, S Ali Beyramabadi","doi":"10.2174/0113862073331831241015103725","DOIUrl":"https://doi.org/10.2174/0113862073331831241015103725","url":null,"abstract":"<p><strong>Aims: </strong>This study aims explore the impact of catechol, dopamine, and L-DOPA on the stability and toxicity of β-amyloid peptides, which play a key role in the neurodegenerative process of Alzheimer's disease, to assess their potential as therapeutic agents.</p><p><strong>Background: </strong>Alzheimer's disease is marked by the aggregation of β-amyloid peptides, which contribute to neurodegeneration. Exploring how various compounds interact with β-amyloid peptides can offer valuable insights into potential therapeutic strategies.</p><p><strong>Objective: </strong>The objective of this research is to explore the interaction mechanisms of catechol, dopamine, and L-DOPA with β-amyloid peptides and assess their impact on peptide stability and aggregation.</p><p><strong>Method: </strong>This study employs molecular dynamics simulations combined with density functional theory to investigate the interactions between β-amyloid and the three compounds. It evaluates changes in peptide stability and salt bridge lengths and performs electronic structure analyses using the Electron Localization Function (ELF) and Harmonic Oscillator Model of Aromaticity (HOMA).</p><p><strong>Results: </strong>The findings reveal that β-amyloid stability decreases significantly when interacting with dopamine and L-DOPA compared to catechol. All three compounds inhibit β-amyloid, with dopamine and L-DOPA showing stronger effects. Catechol primarily interacts through hydrophobic interactions, while dopamine and L-DOPA also form hydrogen bonds with β-amyloid. Electronic structure analysis shows catechol has higher electron localization and anti-aromatic character, affecting its interactions differently than dopamine and L-DOPA. A decrease in the HOMO-LUMO gap from catechol to L-DOPA to dopamine indicates increasing reactivity towards β-amyloid.</p><p><strong>Conclusion: </strong>Dopamine and L-DOPA more effectively disrupt β-amyloid aggregation than catechol, likely due to additional hydrogen bonding and increased electronic reactivity. These insights are crucial for developing therapeutic strategies targeting β-amyloid aggregation in Alzheimer's disease, emphasizing the importance of molecular interactions in modulating peptide stability and toxicity. The study also provides a comparative analysis of the electronic properties and interaction dynamics of the compounds, which can guide future research in the design of β-amyloid inhibitors. The utilization of advanced simulation techniques underscores the potential for computational methods in understanding complex biological interactions and developing novel therapeutic agents. Furthermore, the insights into the differential effects of hydrophobic interactions versus hydrogen bonding offer valuable information for the synthesis of new compounds aimed at mitigating β-amyloid toxicity.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930817","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":"Ferroptosis-related Biotargets and Network Mechanisms of Maslinic Acid Against Myocardial Ischemia-reperfusion Injury: An Integrated Bioinformatic and Experimental Approach.","authors":"Qi Li, Guiyuan He, Rujie Zheng, Chunlei Liu, Che Wang, Zhihao Liu, Zhuqing Li, Chengzhi Lu","doi":"10.2174/0113862073354768241217162514","DOIUrl":"https://doi.org/10.2174/0113862073354768241217162514","url":null,"abstract":"<p><strong>Background: </strong>Maslinic acid (MA), a pentacyclic triterpenoid compound derived from leaves and fruits of Olea europaea, bears multi-pharmacological properties. Our previous studies found that MA exerted a cardioprotective effect by modulating oxidative stress, inflammation, and apoptosis during myocardial ischemia-reperfusion injury (MIRI). Nevertheless, data regarding the anti-ferroptosis effects of MA on MI/RI remains unidentified.</p><p><strong>Aim of the study: </strong>This study aimed to explore the effects of MA on ferroptosis induced by MI/RI, with a focus on elucidating the underlying mechanisms through an integrated approach of network pharmacology and experimental validation.</p><p><strong>Materials and methods: </strong>Several public databases and a protein-protein interaction (PPI) network were used to identify the core targets shared by MI/RI, ferroptosis, and MA. The molecular function, cell component, biological process, and potential signaling pathways of core genes were analyzed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. Subsequently, molecular docking and in vitro experiments were carried out to further validate network pharmacology results.</p><p><strong>Results: </strong>A total of 21 unique intersection genes were obtained as potential targets of MA in treating MI/RI-induced ferroptosis. The 10 hub genes with the highest interaction scores were identified from PPI analysis. GO and KEGG enrichment showed the contribution of the core genes to pharmacological actions and mechanisms in MA treatment of MI/RI, especially the ferroptosis-related signaling pathways. Additionally, MA docked well with ranked core targets, including MAPK, MTOR, STAT3, PTGS2, and MDM2. Subsequently, in vitro experiments revealed that MA notably alleviated oxidative damage, reduced ferrous iron overload and ferroptosis, and regulated the expression of ferroptosis-related genes (GPX4, PTGS2, and ACSL4) in erastin-induced H9c2 cells. Meanwhile, MA could significantly reduce phosphorylation of MAPK (ERK1/2) levels in H9c2 cells.</p><p><strong>Conclusion: </strong>By utilizing network pharmacology and experimental data, our study revealed the correlation between MA and ferroptosis following MI/RI, and concluded that MA might protect against MI/RI by reducing ferroptosis through the ERK1/2 signaling pathway. This finding offered fresh insights into the pharmacological mechanisms of MA against MI/RI.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930569","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":"Verification of Qianlong Shutong Formula in the Treatment of Benign Prostatic Hyperplasia.","authors":"Ze-Chao Zhang, Min Zhu, Shu-Ping Huang, Zhi-Feng Wei, Yu Chen, Chang-Jie Shang","doi":"10.2174/0113862073336172241220182220","DOIUrl":"https://doi.org/10.2174/0113862073336172241220182220","url":null,"abstract":"<p><strong>Aims: </strong>To investigate the mechanisms through which Qianlong Shutong Formula (QLSTF) exerts its effects on the management of benign prostatic hyperplasia (BPH).</p><p><strong>Background: </strong>BPH is a prevalent condition among older men and poses significant management challenges due to the limited effectiveness and potential side effects associated with current treatment options. QLSTF, a traditional Chinese medicine, has been utilized in the treatment of BPH; however, its mechanism of action remains inadequately understood.</p><p><strong>Objective: </strong>This study aimed to identify potential therapeutic targets of QLSTF for the management of BPH through the application of network pharmacology and subsequent experimental validation.</p><p><strong>Methods: </strong>QLSTF compounds were identified utilizing liquid chromatography-mass spectrometry (LC-MS). Potential targets of QLSTF, as well as BPH-related targets, were retrieved from public databases. Crucial bioactive ingredients, potential targets, and signaling pathways were acquired through bioinformatics analysis, including protein-protein interaction (PPI), as well as the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Subsequently, molecular docking was carried out to predict the combination of active compounds with core targets. Lastly, in vitro and in vivo experiments were conducted to further verify the findings.</p><p><strong>Results: </strong>A total of 52 bioactive ingredients of QLSTF and 760 QLSTF-BPH-related targets were screened. Bioinformatics analysis revealed that Afzelin, Ononin, Glycitin, Emodin and Erythritol may be potential candidate agents. AKT1, SRC, STAT3, GRB2, HRAS, MAPK3, PIK3CA, PIK3R1, HSP90AA1, and EP300 could become potential therapeutic targets. PI3KAKT signaling pathway might play an important role in QLSTF against BPH. Moreover, molecular docking suggested that Afzelin, Ononin, Glycitin, Emodin, and Erythritol combined well with AKT1, SRC, STAT3, HRAS, MAPK3, PIK3CA, and PIK3R1, respectively. In vitro and in vivo experiments showed that QLSTF could inhibit the proliferation of cells, as well as the PI3K-Akt signaling pathway, which further confirmed the prediction by network pharmacology strategy and molecular docking.</p><p><strong>Conclusions: </strong>QLSTF may exert its therapeutic effects on BPH by modulating the PI3K/AKT signaling pathway and inhibiting glandular hyperplasia. This study offers valuable insights into the therapeutic targets of QLSTF in the management of BPH.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930818","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":"Nanomaterials for Temporomandibular Joint Osteoarthritis Therapy: A Mini-Review.","authors":"Lulu Chen, Chengcheng Liao","doi":"10.2174/0113862073339608241214053500","DOIUrl":"https://doi.org/10.2174/0113862073339608241214053500","url":null,"abstract":"<p><p>Osteoarthritis, particularly temporomandibular joint (TMJ) osteoarthritis (OA), poses significant challenges in diagnosis and treatment. Recent studies suggest that nanomaterials hold considerable promise in treating TMJ-OA, showing validated efficacy in animal models. However, further research is required to ensure their long-term safety within the TMJ-OA environment. Nanomaterials can facilitate drug delivery and encapsulate functional cells and extracellular vesicles, offering new avenues for exploration. This paper reviews the current research status of nanomaterials in TMJ-OA treatment, including drug delivery, anti-inflammatory, lubricating and buffering, antioxidant, tissue regeneration, scaffold, and stimuli-responsive nanomaterials. Additionally, the paper explores the development and future prospects of nanomaterials in TMJOA treatment, highlighting their unique contributions and aiming to provide new perspectives and solutions for unexplored areas.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930816","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":"Network Pharmacology Combined with Animal Models to Investigate the Mechanism of ChangPu YuJin Tang in the Treatment of Tourette Syndrome.","authors":"Man-Qi Lu, Zheng-Gang Shi, Jing Shang, Lei Gao, Wei-Jiao Gao, Lu Gao","doi":"10.2174/0113862073295447240430113053","DOIUrl":"10.2174/0113862073295447240430113053","url":null,"abstract":"<p><strong>Background: </strong>ChangPu YuJin Tang (CPYJT) is a Chinese herbal formula that has been shown to be an effective therapeutic strategy for pediatric patients with Tourette Syndrome (TS). Using an integrated strategy of network pharmacology and animal model, the aim of this study was to investigate the mechanism of CPYJT in the treatment of TS.</p><p><strong>Methods: </strong>Compound libraries of CPYJT were established using databases, such as the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). The TCMSP database and Swiss Target Prediction database were used to predict the targets. The above results were constructed into a CPYJT-Drug-Component-Target network. Moreover, TS targets were predicted using GeneCards and other databases. The targets corresponding to the potential ingredients in CPYJT and the targets corresponding to TS were taken as the intersections to construct the CPYJT-TS network. The target network was analysed by PPI using the string database. GO and KEGG enrichment analyses were performed on the target network. The whole process was performed using Cytoscape 3.7.2 to make visual network diagrams of the results. CPYJT was characterised by Ultra-Performance Liquid Chromatography-Tandem Mass Spectrometry (UHPLC-MS). Transmission Electron Microscopy (TEM) was used to observe the structural changes of CPYJT on the neuronal cells of the IDPN model rats. RT-PCR and Western Blot were used to analyse the changes in the mRNA and protein expression levels of BDNF, TrkB, PI3K, and AKT in the cortex, striatum, and thalamus brain regions after CPYJT administration in IDPN model rats.</p><p><strong>Results: </strong>Network pharmacology and UHPLC-MS studies revealed that CPYJT acted on the TS through multiple neurotransmitters and the BDNF/TrkB and PI3K/AKT signalling pathways. CPYJT ameliorated neurocellular structural damage in the cortex, striatum, and thalamus of TS model rats. Additionally, CPYJT up-regulated the levels of BDNF, TrkB, PI3k, and AKT in the cortex, striatum, and thalamus of TS model rats.</p><p><strong>Conclusion: </strong>It was found that CPYJT protected neuronal cells from structural damage in multiple brain regions and affected the expression levels of BDNF, TrkB, PI3K, and Akt in the cortex, striatum, and thalamus during TS treatment.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":"166-184"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11826910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140854077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Network Pharmacology and <i>In-silico</i> Approaches to Decipher the Pharmacological Mechanism of <i>Dioscorea septemloba</i> Thunb in Treating Gout and Its Complications.","authors":"Wen-Bin Liu, Jie Dai, Xuan Chen, Ning Du, Jian Hu","doi":"10.2174/0113862073258523231025095117","DOIUrl":"10.2174/0113862073258523231025095117","url":null,"abstract":"<p><strong>Background: </strong>Dioscorea septemloba Thunb. (DST) has demonstrated therapeutic potential in the treatment of gout and its associated complications. However, the underlying mechanisms of DST's pharmacological activity remain unclear. This study aims to investigate the pharmacological substances and network regulatory mechanisms of DST in treating gout and its complications using network pharmacology.</p><p><strong>Methods: </strong>According to ultra-high performance liquid chromatography coupled with hybrid quadrupole-Orbitrap mass spectrometry (UPLC-Q-Exactive Orbitrap-MS) data and Lipinski's rule of five, 24 bioactive phytochemicals from DST were identified. The targets of gout were retrieved from Gene Expression Omnibus (GEO), GeneCards, and DisGeNET databases, followed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG pathway) enrichment analysis. The Cytoscape network analysis was used to identify the primary pathological pathways and key targets. Finally, LeDock was used for molecular docking to verify the active components of DST and their core target proteins.</p><p><strong>Results: </strong>DST contains several core active ingredients, such as tetrahydroimidazo[1,2-a]pyridine- 2,5-dione, diosgenin, beta-sitosterol, dioscorol B, montroumarin and 9,10-dihydro-5,7- dimethoxy-3,4-phenanthrenediol. Moreover, these active components were found to strongly bind to the key targets for treating gout and its complications, including HSP90AA1, STAT3, PTGS2, PPARG, MTOR, HIF1A, MMP9, ESR1, and TLR4. As a result, DST alleviates gout and its complications by inhibiting xanthine dehydrogenase (XDH) to reduce uric acid levels and regulating the HIF-1α, EZH2/STAT3, and COX-2/PPAR-γ pathways to reduce inflammation. Additionally, it also plays an analgesic role by regulating the neuroactive ligand-receptor interaction pathway and calcium ion signaling pathway.</p><p><strong>Conclusion: </strong>This study has provided insights into the underlying mechanisms of DST in the treatment of gout and its complications, which could serve as a scientific foundation for its clinical translation.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":"74-88"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92153010","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":"Inhibition of Taurine-upregulated Gene 1 Upregulates MiR-34a-5p to Protect against Myocardial Ischemia/Reperfusion <i>via</i> Autophagy Regulation.","authors":"Qunjun Duan, Aiqiang Dong, Haifeng Cheng, Shufen Zhang, Wei Chen, Weijun Yang","doi":"10.2174/0113862073267559231106074309","DOIUrl":"10.2174/0113862073267559231106074309","url":null,"abstract":"<p><strong>Background: </strong>Taurine upregulated gene 1 (TUG1) has been identified on long noncoding RNA (lncRNA); however, its function in myocardial cells following ischemia/ reperfusion (I/R) injury has not been explored. This study aimed to investigate the role of LncTUG1 in I/R injury by focusing on its relationship with autophagy induction by regulating miR-34a-5p expression.</p><p><strong>Methods: </strong>We established a myocardial I/R model and H9C2 hypoxia-ischemic and reoxygenation (HI/R) conditions to induce I/R injury. TTC, Western blot, CCK-8 assay, quantitative reverse transcription PCR, flow cytometry, and confocal microscopy were used to assess the size of myocardial infarct, level of some apoptotic-related and autophagy-associated proteins, cell viability, the level of LncRNA TUG1, apoptosis, and autophagy, respectively.</p><p><strong>Results: </strong>The results revealed that a TUG1 knockdown protected against I/R-induced myocardial injury by decreasing the impairment in cardiac function. LncRNA TUG1 expression was increased in a myocardial I/R model and HI/R in H9C2 cells. Moreover, inhibition of LncTUG1 enhanced H9C2 cell viability and protected the cells from HI/R-induced apoptosis. Silencing LncRNA TUG1 promoted HI/R-induced autophagy. Furthermore, TUG1 siRNA upregulated the level of miR-34a-5p compared to the HI/R group. The protective effect of LncRNA TUG1 inhibition on H9C2 cells following HI/R was eliminated by blocking autophagy with an miR-34a-5p inhibitor.</p><p><strong>Conclusion: </strong>These findings indicated that inhibiting TUG1 may reduce the extent of myocardial I/R injury by regulating miR-34a-5p. Taken together, these results suggest that LncRNA TUG1 may represent a novel therapeutic target for myocardial I/R injury.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":"110-121"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139650387","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":"<i>Fructus mori</i>: An Updated Review on Botany, Phytonutrient, Detection, Bioactivity, Quality Marker, and Application.","authors":"Ling-Na Li","doi":"10.2174/0113862073270666231206093528","DOIUrl":"10.2174/0113862073270666231206093528","url":null,"abstract":"<p><strong>Background: </strong><i>Fructus mori</i> (mulberry) is not only a delicious fruit with rich phytonutrients and health functions but also a medicinal plant with many clinical therapeutic values for tonifying kidneys and consolidating essence, making hair black and eyes bright.</p><p><strong>Methods: </strong>The related references about <i>F. mori</i> in this review from 1996 to 2022 had been collected from both online and offline databases, including PubMed, Elsevier, SciFinder, Willy, SciHub, Scopus, Web of Science, ScienceDirect, SpringerLink, Google Scholar, Baidu Scholar, ACS publications, and CNKI. The other information was acquired from ancient books and classical works about <i>F. mori</i>.</p><p><strong>Results: </strong>An updated summary of phytonutrients from <i>F. mori</i> was listed as fellows: flavonoids (1-20) (23.5%), phenolic acids (21-34) 16.5%), alkaloids (35-75) (48.2%), polysaccharides (76- 78) (3.5%), other compounds (79-85) (8.3%). The above chemical components were detected by TLC, UV-Vis, HPLC, GC-MS, and AAS methods for their quality standards. The various bioactivities (hepatoprotective, immunomodulatory, anti-oxidant, hypoglycemic, anti-cancer, and other activities) of mulberry are summarized and discussed in this review, which laid an important basis for analyzing their mechanisms and quality markers. This review summarized its applications for vinegar, wine, yogurt, drink, jelly, and sweetmeat in food fields, and the existing problems and future development directions are also discussed in this review.</p><p><strong>Conclusions: </strong>This review made a comprehensive description of <i>F. mori</i>, including botany, phytonutrient, detection, bioactivity, quality marker, and application. It will not only provide some important clues for further studying <i>F. mori,</i> but also provide some valuable suggestions for in-depth research and development of <i>F. mori</i>.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":"12-32"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139566893","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":"Jeduxiaoliu Formula can Induce Apoptosis of Lymphoma Cells <i>In Vitro</i> and <i>In Vivo</i>.","authors":"XiaoWei Feng, Ming Hu, Cong Ming Wei, Hong Yu Zhang, Wen Wen Jiang, Qi Hu","doi":"10.2174/0113862073271687231122064637","DOIUrl":"10.2174/0113862073271687231122064637","url":null,"abstract":"<p><strong>Objective: </strong>Lymphoma is the most common malignancy of the haematological system. Jeduxiaoliu formula (JDXLF) exerts good therapeutic effects against lymphoma, however, the mechanisms underlying these effects remain unclear. Therefore, this study aimed to investigate the mechanism of action of JDXLF.</p><p><strong>Methods: </strong>RNA-Seq was performed to examine the molecular mechanisms underlying the therapeutic effects of JDXLF against lymphoma. CCK-8 assay was performed to examine the effects of JDXLF on the proliferation of lymphoma cells. Electron microscopy was performed to examine the morphology of lymphoma cells. Flow cytometry was performed to examine the apoptosis and cell cycle of lymphoma cells. qPCR and Western blotting were performed to detect the expression of apoptotic genes and proteins. <i>In vivo</i>, the tumour-suppressive effect of JDXLF on lymphoma transplanted tumours was examined by establishing a subcutaneous transplantation tumour model in nude mice, and the expression of apoptotic proteins in tumour tissues was analysed via immunohistochemical staining.</p><p><strong>Results: </strong>RNA-Seq revealed 71, 350 and 620 differentially expressed genes (DEGs) in the 1 mg/mL, 4 mg/mL and 8 mg/mL JDXLF treatment groups, respectively. KEGG pathway analysis showed that the DEGs were significantly associated with apoptosis, TNF signalling and NF-κB signalling. <i>In vitro</i> experiments revealed that JDXLF inhibited the proliferation of lymphoma (Raji and Jeko-1) cells in a dose-dependent manner, induced apoptosis and upregulated the expression of Bax/Bcl2 and caspase3. <i>In vivo</i> experiments revealed that JDXLF had a significant tumourshrinking effect on mice and increased the expression of the apoptosis-related proteins caspase3 and Bax/Bcl2.</p><p><strong>Cconclusions: </strong>This study indicates that JDXLF can induce apoptosis in lymphoma cells <i>in vitro</i> and <i>in vivo</i>. We suggest this may provide a direction for further research into lymphoma therapy.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":"319-338"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139416486","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}