Cell Biochemistry and Biophysics最新文献

{"title":"Role of circRNAs in regulating cell death in cancer: a comprehensive review.","authors":"Mohamed J Saadh, Hadi Mohammed Ehymayed, Tuqa S Alazzawi, Ali A Fahdil, Zainab H Athab, Bekhzod Yarmukhamedov, Hayder Hamid Abbas Al-Anbari, Mohammed Mohsin Shallal, Fahad Alsaikhan, Bagher Farhood","doi":"10.1007/s12013-024-01492-6","DOIUrl":"https://doi.org/10.1007/s12013-024-01492-6","url":null,"abstract":"<p><p>Despite multiple diagnostic and therapeutic advances, including surgery, radiation therapy, and chemotherapy, cancer preserved its spot as a global health concern. Prompt cancer diagnosis, treatment, and prognosis depend on the discovery of new biomarkers and therapeutic strategies. Circular RNAs (circRNAs) are considered as a stable, conserved, abundant, and varied group of RNA molecules that perform multiple roles such as gene regulation. There is evidence that circRNAs interact with RNA-binding proteins, especially capturing miRNAs. An extensive amount of research has presented the substantial contribution of circRNAs in various types of cancer. To fully understand the linkage between circRNAs and cancer growth as a consequence of various cell death processes, including autophagy, ferroptosis, and apoptosis, more research is necessary. The expression of circRNAs could be controlled to limit the occurrence and growth of cancer, providing a more encouraging method of cancer treatment. Consequently, it is critical to understand how circRNAs affect various forms of cancer cell death and evaluate whether circRNAs could be used as targets to induce tumor death and increase the efficacy of chemotherapy. The current study aims to review and comprehend the effects that circular RNAs exert on cell apoptosis, autophagy, and ferroptosis in cancer to investigate potential cancer treatment targets.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142144860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TREM2 Impairs Glycolysis to Interrupt Microglial M1 Polarization and Inflammation via JAK2/STAT3 Axis.","authors":"Chanyuan Liu, Xueying Zhou","doi":"10.1007/s12013-024-01520-5","DOIUrl":"https://doi.org/10.1007/s12013-024-01520-5","url":null,"abstract":"<p><p>Cerebral ischemia/reperfusion injury (IRI) is a primary pathophysiological basis of ischemic stroke, a dreadful cerebrovascular event carrying substantial disability and lethality. Triggering receptor expressed on myeloid cells 2 (TREM2) is a membrane glycoprotein that has been notified as a protective factor for cerebral ischemic stroke. On this basis, the paper is thereby goaled to interpret the probable activity and downstream mechanism of TREM2 against cerebral IRI. Cerebral IRI was simulated in murine microglial BV2 cells under oxygen-glucose deprivation and reperfusion (OGD/R) conditions. Western blotting ascertained the expressions of TREM2 and janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) axis-associated proteins. ELISA and RT-qPCR assayed the secretion of inflammatory cytokines. Immunofluorescence and western blotting estimated macrophage polarization. Glycolysis activation was measured through evaluating lactic acid and extracellular acidification rate (ECAR). RT-qPCR and western blotting examined the expressions of glycolytic genes. TREM2 was abnormally expressed and JAK2/STAT3 axis was aberrantly activated in BV2 cells in response to OGD/R. Elevation of TREM2 repressed the inflammatory reaction and glycolysis, inhibited the JAK2/STAT3 axis, whereas promoted M1-to-M2 polarization in OGD/R-injured BV2 cells. Upregulated TREM2 inactivated the glycolytic pathway to relieve OGD/R-induced inflammatory injury and M1 macrophage polarization. Besides, STAT3 activator, colivelin, aggravated the glycolysis, inflammatory injury and drove M1-like macrophage polarization in TREM2-overexpressing BV2 cells exposed to OGD/R. Collectively, TREM2 might produce anti-inflammatory potential in cerebral IRI, which might dependent on the inactivation of glycolytic pathway via intermediating the JAK2/STAT3 axis.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142138932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture Ameliorates Neuronal Damage and Neurological Deficits after Cerebral Ischemia-Reperfusion Injury via Restoring Telomerase Reverse Transcriptase.","authors":"Dan Chen, Yunxia Xiang, Di Wu, Hui Wang, Yaping Huang, Hongbo Xiao","doi":"10.1007/s12013-024-01504-5","DOIUrl":"https://doi.org/10.1007/s12013-024-01504-5","url":null,"abstract":"<p><p>The purpose of this study is to identify the therapeutic effect of electroacupuncture (EA) on cerebral ischemia-reperfusion (I/R) injury, and to clarify the regulatory mechanism related to telomerase reverse transcriptase (TERT)-mediated telomerase activity. A Middle cerebral artery occlusion/reperfusion (MCAO/R) animal model was constructed and rats were treated by EA invention at the Baihui (GV20) and Fengchi (GB20) acupoints. Neurological deficits were assessed via rotarod test and Morris water maze test. 2,3,5-Triphenyltertrazolium chloride (TTC) staining was performed to evaluate infarct volume. Histological changes were observed under H&E staining and Nissl staining. TERT expression was examined using qRT-PCR and western blot. Telomerase activity was assessed with TRAP method. Neuron apoptosis and senescence were assessed by TUNEL and immunofluorescence assays. Inflammatory cytokines and oxidative stress-indicators were examined using commercial kits. EA intervention at both GV20 and GB20 acupoints reduced infarct volumes (2.48 ± 1.89 vs. 29.56 ± 2.55), elevated the telomerase activity (0.84 ± 0.08 vs. 0.34 ± 0.09), and upregulated the levels of total TERT protein (0.61 ± 0.09 vs. 0.21 ± 0.05) and mitochondrial TERT (Mito-TERT; 0.54 ± 0.03 vs. 0.27 ± 0.03) in hippocampus tissues of MCAO/R rats. EA intervention attenuated motor dysfunction (112.00 ± 6.69 vs. 30.02 ± 2.60) and improved spatial learning (23.87 ± 1.90 vs. 16.23 ± 1.45) and memory ability (8.38 ± 1.06 vs. 4.13 ± 1.13) of rats with cerebral I/R injury. In addition, EA intervention significantly attenuated histopathological changes of injured neurons, mitigated neuron apoptosis (32.27 ± 5.52 vs. 65.83 ± 4.31) and senescence in MCAO/R rats, as well as inhibited excessive production of inflammatory cytokines and attenuated oxidative stress. However, the above therapeutic efficiency of EA intervention in MCAO/R rats was partly eliminated by TERT knockdown. EA intervention at GB20 and GV20 acupoints exerted a protective role in cerebral I/R injury partly through restoring TERT function, implying the clinical potential of EA treatment in the treatment of ischemic stroke.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics analysis of the lipid-regulating effects of metformin in a glucose concentration-dependent manner in macrophage-derived foam cells.","authors":"Jie Qi, Mengya Dong, Qiling Gou, Huolan Zhu","doi":"10.1007/s12013-024-01269-x","DOIUrl":"https://doi.org/10.1007/s12013-024-01269-x","url":null,"abstract":"<p><p>Metformin has a long history of clinical application and has been shown to have outstanding ability in lowering glucose. Recent advances have further revealed its broad modulatory ability beyond glucose-lowering, expanding the scope of metformin applications. Metformin has now been applied as a viable lipid-lowering strategy in non-hyperglycemic obese patients. However, the benefits and underlying pharmacological mechanisms of metformin administration in non-hyperglycemic populations remain to be explained. Our study aimed to systematically investigate the differences in the lipid-lowering function and pharmacological mechanisms of metformin in high- and low-sugar conditions to facilitate the development of individualized metformin use regimens for different clinical patients. We constructed macrophage-derived foam cell models in vitro for subsequent analysis. ORO results showed that metformin significantly reduced lipid accumulation in macrophages in both high and low glucose environments, but the lipid decline was higher in the high glucose environment. By mutual validation and joint analysis of transcriptomics and metabolomics, significant differences in metformin transcriptional and metabolic patterns existed among high and normal glucose environments. The significant alterations of genes such as DGKA, LPL, DGAT2 and lipid metabolites such as LysPA and LysPC partially explained the glucose-dependent pharmacological function of metformin. In conclusion, our study confirmed that the lipid-lowering effect of metformin depends on the extracellular glucose concentration, and systematically studied the molecular mechanism of metformin in different glycemic environments, which provides a certain reference value for the subsequent in-depth study and clinical application.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pomegranate Peel Extract as 6-Phosphogluconate Dehydrogenase (6PGD) Inhibitor for Treatment of Breast Cancer.","authors":"Saba Riaz, Azhar Rasul, Matloob Ahmad, Muhammad Asrar, Mudassir Hassan","doi":"10.1007/s12013-024-01485-5","DOIUrl":"https://doi.org/10.1007/s12013-024-01485-5","url":null,"abstract":"<p><p>Targeting the enzymes of Pentose Phosphate Pathway (PPP) has been emerged as a novel strategy for treatment of cancer. 6-phosphogluconate dehydrogenase (6PGD) is third enzyme of PPP and converts 6-phosphogluconate (6-PG) into ribulose 5-phosphate (R-5-P) and produces NADPH. The overexpression of 6PGD has been reported in many human cancers especially in breast cancer and is emerged as the potential anti-cancer drug target. The current study is focused to screen an already established library of plant extracts against 6PGD, among which Pomegranate peel extract showed significant 6PGD inhibitory activity with IC50 value = 0.090 μg/mL. Pomegranate peel competitively inhibited NADP+ and 6-phosphogluconate to 6PGD enzyme having Ki constant value = 12.72 ± 5.54 ng/mL. Moreover, anti-breast cancer activity against MCF-7 cells determined Pomegranate peel as the potent inhibitor of cancerous cells with IC50 value = 3.138 μg/mL. Toxicity profiling of pomegranate peel extract (2000mg/kg) did not show any adverse effect on mice. Moreover, Ont the base of literature a library of known compounds of pomegranate was prepared and established and screened against 6PGD for the identification of actual responsible phytochemicals of 6PGD activity by using molecular docking. Computational tools were used to evaluate selected potent hits. Out of 26 compounds, three potent phytochemicals (Procyanidin, Delphinidin and Cyanidin) exhibited the best binding affinities with 6PGD. In addition, these phytochemicals displayed the best favorable hydrogen bonding, binding energy, and protein-ligand interactions as compare to 3PG. Molecular dynamics simulation suggested that these hits form a stable binding complex with the active site of 6PGD. These findings suggest that Pomegranate peel and its secondary metabolites as the potent inhibitors of 6PGD and the best drug candidate for treatment of breast cancer.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAFs-derived Exosomal miR-889-3p Might Repress M1 Macrophage Polarization to Boost ESCC Development by Regulating STAT1.","authors":"Shaofeng Zhang, Danqing Li, Haijun Wang, Bo Liu, Fan Du, Qing Wang","doi":"10.1007/s12013-024-01496-2","DOIUrl":"https://doi.org/10.1007/s12013-024-01496-2","url":null,"abstract":"<p><p>Cancer-associated fibroblasts (CAFs) represent one of the major components of the tumor stroma, which might create an immunosuppressive tumor microenvironment by inducing and functionally polarizing protumoral macrophages. Previous studies indicated that exosomes derived from CAFs might transmit regulating signals and boost esophageal squamous cell carcinoma (ESCC) development. This study is designed to explore the role and mechanism of CAFs-derived exosomal microRNA-889-3p (miR-889-3p) in ESCC progression. Macrophage polarization was detected using flow cytometry. miR-889-3p, Tumor necrosis factor alpha (TNF-α), and inducible nitric oxide synthase (iNOS) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, cycle progression, migration, and invasion were assessed using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), scratch assay, and Transwell assays. α-SMA, FAP, CD63, CD81, and signal transducer and activator of transcription 1 (STAT1) protein levels were detected using western blot. Exosomes were characterized using an electron microscope and nanoparticle tracking analysis (NTA). Binding between miR-889-3p and STAT1 was predicted by Starbase, and verified by a dual-luciferase reporter and RNA pull-down. The effect of CAFs-derived exosomal miR-889-3p on ESCC tumor growth in vivo was detected using mice xenograft assay. miR-889-3p level was decreased in LPS-induced M0 macrophages. CAF-derived exosomal miR-889-3p knockdown suppressed ESCC proliferation, migration, and invasion. CAFs might transfer miR-889-3p to M0 macrophages via exosomes. STAT1 was a target of miR-889-3p. Besides, in vivo studies confirmed that CAFs-derived exosomal miR-889-3p can accelerate ESCC tumor growth by regulating STAT1. CAFs-derived exosomal miR-889-3p facilitates esophageal squamous cell carcinoma cell proliferation, migration, and invasion by inhibiting M1 macrophage polarization through down-regulation of STAT1, providing a promising therapeutic target for ESCC.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142138931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural Insight on Interaction of NMDA receptor with fentanyl, ketamine and Isoflurane: A Computational Study to Unravel Mode of Binding.","authors":"Atif Khalid, Nabeela Farhat","doi":"10.1007/s12013-024-01499-z","DOIUrl":"https://doi.org/10.1007/s12013-024-01499-z","url":null,"abstract":"<p><p>NMDA receptors are considered targets for many anesthetics if they are modulated by the drugs at clinically relevant concentrations. Volatile anesthetics like isoflurane and ketamine interact with NMDA receptors, inhibiting channel activation and thus blocking NMDA neurotransmission at clinically relevant concentrations. The mode of binding of commonly used drugs like ketamine, isoflurane, and fentanyl is poorly understood. We used molecular docking, molecular dynamics simulations, and DFT calculation of these drugs against the NMDA receptor. Using well-defined computational methods, we identified that these drugs have high docking scores and significant interaction with receptors. These drugs bind to the substrate-binding pocket and form a remarkable number of interactions. We have found that these interactions are stable and have low HOMO-LUMO energy gaps. This study provides enough evidences of strong and stable interaction between drugs and NMDA receptor.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual Role of Extracellular Vesicles as Orchestrators of Emerging and Reemerging Virus Infections.","authors":"A P Athira, Smrithi Sreekanth, Ananthu Chandran, Anismrita Lahon","doi":"10.1007/s12013-024-01495-3","DOIUrl":"https://doi.org/10.1007/s12013-024-01495-3","url":null,"abstract":"<p><p>Current decade witnessed the emergence and re-emergence of many viruses, which affected public health significantly. Viruses mainly utilize host cell machinery to promote its growth, and spread of these diseases. Numerous factors influence virus-host cell interactions, of which extracellular vesicles play an important role, where they transfer information both locally and distally by enclosing viral and host-derived proteins and RNAs as their cargo. Thus, they play a dual role in mediating virus infections by promoting virus dissemination and evoking immune responses in host organisms. Moreover, it acts as a double-edged sword during these infections. Advances in extracellular vesicles regulating emerging and reemerging virus infections, particularly in the context of SARS-CoV-2, Dengue, Ebola, Zika, Chikungunya, West Nile, and Japanese Encephalitis viruses are discussed in this review.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal Non-coding RNA Derived from Mesenchymal Stem Cells (MSCs) in Autoimmune Diseases Progression and Therapy; an Updated Review.","authors":"Shireen Hamid Farhan, Saade Abdalkareem Jasim, Pooja Bansal, Harpreet Kaur, Mohammed Abed Jawad, Maytham T Qasim, Abeer Mhussan Jabbar, Mahamedha Deorari, Ahmed Alawadi, Ali Hadi","doi":"10.1007/s12013-024-01432-4","DOIUrl":"https://doi.org/10.1007/s12013-024-01432-4","url":null,"abstract":"<p><p>Inflammation and autoimmune diseases (AD) are common outcomes of an overactive immune system. Inflammation occurs due to the immune system reacting to damaging stimuli. Exosomes are being recognized as an advanced therapeutic approach for addressing an overactive immune system, positioning them as a promising option for treating AD. Mesenchymal stem cells (MSCs) release exosomes that have strong immunomodulatory effects, influenced by their cell of origin. MSCs-exosomes, being a cell-free therapy, exhibit less toxicity and provoke a diminished immune response compared to cell-based therapies. Exosomal non-coding RNAs (ncRNA), particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are intricately linked to various biological and functional aspects of human health. Exosomal ncRNAs can lead to tissue malfunction, aging, and illnesses when they experience tissue-specific alterations as a result of various internal or external problems. In this study, we will examine current trends in exosomal ncRNA researches regarding AD. Then, therapeutic uses of MSCs-exosomal ncRNA will be outlined, with a particle focus on the underlying molecular mechanisms.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Dynamics Simulation Studies of Beta-Glucogallin and Dihydro Dehydro Coniferyl Alcohol from Syzygium cumini for its Antimicrobial Activity on Staphylococcus aureus.","authors":"N Bhavyashree, M S Vaishnavi, P Shravani, Sasmita Sabat","doi":"10.1007/s12013-024-01489-1","DOIUrl":"https://doi.org/10.1007/s12013-024-01489-1","url":null,"abstract":"<p><p>With the escalating threat of antimicrobial resistance (AMR), discovering novel therapeutic agents against resistant pathogens like Staphylococcus aureus is crucial. This study explores phytochemicals from Syzygium cumini for their potential efficacy against AMR S. aureus infections, elucidating their mechanisms through in silico methods. We investigated 83 compounds from S. cumini, sourced from PubMed, using rigorous docking analysis against the ATP binding domain AgrC of S. aureus with AMdock with Autodock Vina v1.5.2. Drug-likeness predictions were assessed using SwissADME v2023 and Pass online v2.0. Molecular dynamics (MD) simulations identified promising compounds, focusing on stability and interaction dynamics. Beta-Glucogallin (BEG) and Dihydro Dehydro Coniferyl alcohol (DIH) emerged as significant hits. MD simulations with GROMACS v2020.6 revealed stable BEG and DIH complexes with AgrC, forming six hydrogen bonds with six key amino acids (Arg-303, Asp-338, Glu-342, Glu-384, Lys-389, Gly-396), indicating strong and stable bonding. The binding affinities for DIH and BEG are -73.474 ± 11.104 kJ/mol and -6.319 ± 18.823 kJ/mol with 4BXI, respectively. Our findings highlight BEG and DIH as promising candidates against AMR S. aureus infections, showing favourable binding affinities and stable interactions with AgrC. This study underscores the importance of natural products in combating AMR and demonstrates the utility of computational methodologies in drug discovery. Further experimental validation is warranted to fully exploit these phytochemicals' therapeutic potential.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}