Molecular Biology Reports最新文献

{"title":"Differential expression of hsa-miR-21-5p and hsa-miR-26a-5p in oral squamous cell carcinoma: A Single Centre pilot study.","authors":"Sriram Kaliamoorthy, Ganesan Vinitha, Kokila Manickam, Vanidha Kandasamy, Ponranjani C Vedeswari, Sai P Archana","doi":"10.1007/s11033-026-12712-y","DOIUrl":"https://doi.org/10.1007/s11033-026-12712-y","url":null,"abstract":"<p><strong>Purpose: </strong>Oral squamous cell carcinoma (OSCC) is a leading cause of cancer mortality, and reliable molecular markers are needed, particularly in resource-limited settings. This pilot study evaluated the expression of two microRNAs, hsa-miR-21-5p and hsa-miR-26a-5p, in OSCC tissue compared with normal oral tissue, as a hypothesis-generating step toward biomarker development.</p><p><strong>Methods: </strong>In this single-centre case-control pilot study, 16 histopathologically confirmed OSCC tissues and 16 histologically normal control tissues were analysed. Total RNA was extracted and reverse-transcribed, and hsa-miR-21-5p and hsa-miR-26a-5p were quantified by qRT-PCR using U6 snRNA as reference gene and the 2^-ΔΔCt method. Group differences were assessed using the Mann-Whitney U test with Hodges-Lehmann median differences, and receiver operating characteristic (ROC) analysis with bootstrap and leave-one-out internal validation.</p><p><strong>Results: </strong>hsa-miR-26a-5p was consistently upregulated in OSCC (Hodges-Lehmann ΔCt difference 3.59, 95% CI 3.02-4.19; p < 0.001) and completely separated OSCC from controls (AUC 1.000). hsa-miR-21-5p showed a smaller, inconsistent difference (1.21, 95% CI 0.26-1.99; p = 0.012; AUC 0.758). Neither marker was associated with tumour stage, grade, age, or sex. As the cohort comprised only advanced (Stage III-IV) disease within a single sample set, this separation is reported descriptively rather than as validated diagnostic accuracy.</p><p><strong>Conclusion: </strong>hsa-miR-26a-5p is robustly overexpressed in advanced OSCC and warrants validation in larger, independent, stage-diverse cohorts before any diagnostic application, which would require validation is considered.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897547","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":"Therapeutic potential of apigenin in neurodegenerative diseases and brain health.","authors":"Mohannad Aldiqs, Mansur Aliev, Tushar B Gajjar, Jitendra Narayan Senapati, Bahjat Alhasso, Dilbar Urazbaeva, Shakhrijakhon Aminqulov, Manoj Kumar Mishra","doi":"10.1007/s11033-026-12703-z","DOIUrl":"https://doi.org/10.1007/s11033-026-12703-z","url":null,"abstract":"<p><p>Neurodegenerative disorders are characterized by progressive neuronal loss and remain a major global health concern, largely due to their complex and multifactorial nature. These conditions, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, involve overlapping mechanisms such as oxidative stress, chronic inflammation, mitochondrial dysfunction, and impaired neurotransmission. In recent years, natural bioactive compounds have gained attention as potential therapeutic candidates. Among them, apigenin, a dietary flavonoid widely found in fruits and vegetables, exerts neuroprotective effects through multiple cellular pathways. This review highlights the potential role of apigenin in modulating key pathological processes in the central nervous system. Apigenin reduces oxidative stress by scavenging reactive oxygen species and activating endogenous antioxidant systems, particularly through Nrf2 signaling. It also exhibits anti-inflammatory effects by inhibiting pathways such as NF-κB and MAPK, thereby lowering pro-inflammatory cytokine production and regulating microglial activation. In addition, apigenin supports mitochondrial function and inhibits apoptosis by modulating Bcl-2 family proteins and caspase activity. Its role extends beyond maintaining blood-brain barrier integrity to regulating autophagy and mitophagy and enhancing neurotrophin signaling, especially through the BDNF/TrkB pathways. Moreover, apigenin influences neurotransmission by balancing excitatory and inhibitory signaling and modulating cholinergic and monoaminergic systems. Despite promising preclinical findings, its clinical application remains limited due to bioavailability challenges and insufficient human studies.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897590","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":"Anti-cancer efficacy of combined vaccine-strain measles and mumps viruses against colorectal cancer: an experimental study.","authors":"Trinh Xuan Hung, Nguyen Dang Tung, Nguyen Thi Huong, Dong Thai Hoa, Le Duy Cuong","doi":"10.1007/s11033-026-12724-8","DOIUrl":"https://doi.org/10.1007/s11033-026-12724-8","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to evaluate the oncolytic efficacy of a combination of vaccine-strain measles virus (MeV) and mumps virus (MuV) against colorectal cancer (CRC) cells in vitro and in a nude mouse xenograft model.</p><p><strong>Materials and methods: </strong>HT-29 cells were cultured in Dulbecco's Modified Eagle Medium (DMEM) and infected with MeV, MuV, or a combination of MeV and MuV (MM; MeV: MuV = 1:1, v/v). Cell viability, synergistic effects, and apoptosis were assessed using MTT and flow cytometry assays, respectively, in vitro. A nude mouse xenograft model was established to evaluate the in vivo oncolytic efficacy of the MM against CRC xenograft tumors.</p><p><strong>Results: </strong>The MM demonstrated synergistic effects at 48, 72, and 96 h (CI = 0.473, 0.692, and 0.633, respectively). The MM-treated group showed significantly lower cell viability (p < 0.05) and a markedly higher apoptotic rate (p < 0.01) compared with single-virus-infected groups in vitro. In the xenograft model, the MM-treated group exhibited significantly slower tumor growth (p ≤ 0.001), significantly prolonged survival (p < 0.05), reduced mortality, and increased proportions of innate immune cell populations in the spleen compared with single-virus-treated groups.</p><p><strong>Conclusions: </strong>The MM demonstrated synergistic and superior oncolytic efficacy against HT-29 colorectal cancer cells compared with single-virus therapies in both in vitro and in vivo xenograft models.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897498","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":"Interactions between circular RNAs (circRNAs) and the Hippo pathway in cancer.","authors":"Penghui Li, Di Huang, Xinyu Gu","doi":"10.1007/s11033-026-12721-x","DOIUrl":"https://doi.org/10.1007/s11033-026-12721-x","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) have emerged as pivotal regulators in cancer biology, attributed to their stability, abundance, and tissue-specific expression. Dysregulation of the Hippo pathway is associated with various cancers, with circRNAs influencing its activity. These circRNAs exhibit aberrant expression in multiple cancers, correlating with clinical features and prognosis. The interaction between circRNAs and the Hippo signaling pathway highlights their potential as diagnostic and prognostic biomarkers. By modulating Hippo pathway activity, circRNAs significantly impact tumorigenesis and cancer progression. Therapeutic strategies targeting circRNA-Hippo interactions have demonstrated promise in preclinical models. This review delves into the complex roles of circRNAs in Hippo pathway modulation and their implications for cancer progression. Future research should aim to elucidate the mechanisms of circRNA-Hippo interactions comprehensively and translate these insights into clinical applications, thereby advancing cancer diagnosis, prognosis, and treatment. Integrating circRNA profiling into clinical practice could revolutionize cancer management and enhance patient outcomes.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897557","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":"Recent advancements in NRF2-regulated ferroptosis modulation for targeted cancer therapy.","authors":"Ozge Cemiloglu Ulker, Antonella Capozzi, Nisa Nur Sari-Goktas, Maurizio Sorice, Luciano Saso, Brigitta Buttari","doi":"10.1007/s11033-026-12705-x","DOIUrl":"https://doi.org/10.1007/s11033-026-12705-x","url":null,"abstract":"<p><p>The nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway is a major regulator of cellular response to oxidative stress. While NRF2 protects the normal cells against oxidative stress, its abnormal signaling activity in the context of cancer helps tumor cells evade oxidative stress, survive, proliferate, and develop resistance to treatment. Increasing evidence has established the tight connection between NRF2 signaling and ferroptosis, a type of programmed cell death based on iron-dependent lipid oxidation. In this review, the role of NRF2 in regulating important pathways as glutathione metabolism, lipid peroxidation, and iron homeostasis that contribute to the process of ferroptosis is discussed. This review highlights the latest progress that has been made in therapies that are designed to target the NRF2-ferroptosis pathway in cancers, by providing an overview of the mechanism involved as well as relevant pre-clinical and current clinical studies. The latest advancements regarding the NRF2 modulators and ferroptosis inducers, both natural and synthetic, along with new studies regarding the ability of such compounds to overcome drug resistance and increase antitumor effectiveness are reviewed.In addition, it is addressed current studies in biomarker discovery, precision medicine, drug targeting in terms of future direction. Moreover, the existing limitations related to clinical application of NRF2 and ferroptosis modulation therapies are also described, including tumor heterogeneity, treatment selectivity, biomarker validation, and possible toxicity of such therapy to normal tissue.Overall, these developments provide the rationale for the clinical application of the NRF2-ferroptosis pathway as a therapeutic target in overcoming drug resistance.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897616","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":"Mitochondrial dysfunction and apoptosis-related gene activation induced by combined ethyl acetate fractions of Uncaria sp. and Selaginella doederleinii in Saccharomyces cerevisiae.","authors":"Zaidatu Khoirun Nisa, Rika Indri Astuti, Sulistiyani Sulistiyani, Sera Budi Verinda, Syaefudin Suminto","doi":"10.1007/s11033-026-12725-7","DOIUrl":"https://doi.org/10.1007/s11033-026-12725-7","url":null,"abstract":"<p><strong>Background: </strong>The combination of ethyl acetate fractions from Uncaria sp. and Selaginella doederleinii (EAF-BC) holds potential as an anticancer agent; however, its underlying molecular mechanism remains unclear. This study aimed to determine the anticancer potential of these combinations by evaluating the hallmarks of apoptosis using a Saccharomyces cerevisiae model.</p><p><strong>Methods and results: </strong>Yeast cells were incubated with EAF-BC at concentrations of 5, 10, and 100 ppm for 24 h. The analyzed parameters included petite colony frequency, mitochondrial activity, cell surface morphology, phosphatidylserine externalization, DNA fragmentation, and apoptosis-related gene regulation (FSH3, AIF1, and YCA1). The results showed that EAF-BC induced mitochondria-driven apoptosis in a dose-dependent manner. The 100-ppm concentration caused severe mitochondrial damage, yielding 85% petite colony formation, reduced mitochondrial fluorescence, surface wrinkling, phosphatidylserine externalization, and DNA fragmentation. This concentration significantly upregulated FSH3 (6-fold), YCA1 (3-fold), and AIF1 (2-fold) expression. Lower concentrations (5 and 10 ppm) also induced apoptosis, although the activity was lower.</p><p><strong>Conclusion: </strong>EAF-BC induced apoptosis-associated cellular changes accompanied by mitochondrial dysfunction in Saccharomyces cerevisiae, as evidenced by increased petite colony formation and multiple apoptotic hallmarks.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897641","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":"Phylogeographic analysis of Staphylococcus nepalensis reveals global occurrence of antimicrobial-resistant lineages carrying the sal(E) resistance gene.","authors":"Johana Becerra, Isabella Gaião, Roberta Almeida Vincenzi, Davi Gabriel Salustiano Merighi, Felipe Vásquez-Ponce, Santiago Justo Arevalo, Jesus Pariona, Gregory Melocco, Fernanda Esposito, Fabio Rodrigues, Nilton Lincopan","doi":"10.1007/s11033-026-12601-4","DOIUrl":"10.1007/s11033-026-12601-4","url":null,"abstract":"<p><strong>Background: </strong>Staphylococcus nepalensis is an emerging species first described in 2003 from the respiratory tract of goats in Nepal. We report the identification of S. nepalensis of a hypersaline lagoon in Brazil, along with in-depth phylogeographical and resistome analysis of publicly available genomes.</p><p><strong>Methods and results: </strong>During a local survey from hypersaline aquatic environments in Rio de Janeiro, Brazil, two staphylococcal strains were recovered, designated as COLB and AM1. These isolates were subjected to antimicrobial susceptibility testing, genomic sequencing, and comprehensive phylogenomic analyses. Genomic analysis confirmed the taxonomic identity of COLB and AM1 as S. nepalensis. Both isolates harbored the sal(E) conferring resistance to pleuromutilins and streptogramin A, whereas tet(K) conferring to tetracyclines. Additionally, AM1 carried lnu(A), consistent with the reduced susceptibility to clindamycin (MIC = 2 µg/mL) relative to COLB. Genes associated with arsenic and copper tolerance, and the replicons rep7a and rep19c, were confirmed. Phylogenomic analysis indicated that COLB and AM1 were clonally related (1 cgSNP-difference) but distinct from global isolates. Phylogeographic analysis revealed wide geographic occurrence, with some lineages carrying blaZ and mecA associated with beta-lactamase production and methicillin resistance, respectively. Strikingly, sal(E) is conserved across all S. nepalensis genomes.</p><p><strong>Conclusions: </strong>The findings confirm the presence of S. nepalensis in South America as early as 2016 and documented among available genomes from environmental, human, and animal-associated sources. Furthermore, reveal the circulation of some lineages carrying clinically relevant antimicrobial genes, underscoring the importance of accurate species identification and continuous genomic surveillance and potential One Health relevance.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891297","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":"Multifactorial mechanisms of 5-fluorouracil-induced cardiotoxicity and the cardioprotective role of gallic acid.","authors":"Gürkan Imre, Cuneyt Caglayan, Özge Kandemir, Tugba Celik Samanci, Elif Dalkılınç, Sefa Küçükler, Fatih Mehmet Kandemir","doi":"10.1007/s11033-026-12716-8","DOIUrl":"https://doi.org/10.1007/s11033-026-12716-8","url":null,"abstract":"<p><strong>Background: </strong>5-Fluorouracil (5-FU) is an effective chemotherapeutic agent widely used in the treatment of solid tumors; however, its clinical use is limited by cardiotoxicity. This study investigated the molecular mechanisms underlying 5-FU-induced cardiotoxicity and evaluated the potential cardioprotective effects of gallic acid (GA).</p><p><strong>Methods: </strong>Twenty-eight male Wistar albino rats were randomly assigned to four groups (n = 7/group): Control, GA, 5-FU, and 5-FU + GA. GA (120 mg/kg/day, orally) was administered for 7 consecutive days, and a single intraperitoneal dose of 5-FU (150 mg/kg) was given on day 5. Serum cardiac injury markers, cardiac oxidative stress parameters, inflammation-, ER stress-, autophagy-, and apoptosis-related gene expression, PI3K/AKT protein levels, and histopathological and immunohistochemical changes were evaluated.</p><p><strong>Results: </strong>5-FU significantly increased serum LDH and CK-MB levels, oxidative stress, inflammatory, ER stress, autophagy, and apoptosis-related markers, and induced marked histopathological and immunohistochemical alterations in cardiac tissue. Co-treatment with GA markedly ameliorated these biochemical, molecular, and histopathological changes, whereas GA alone produced findings comparable to those of the control group.</p><p><strong>Conclusions: </strong>GA protects against 5-FU-induced cardiotoxicity by attenuating oxidative stress, inflammation, ER stress, autophagy, and apoptosis, suggesting its potential as a cardioprotective adjunct during 5-FU chemotherapy.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890804","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":"PTBP1 at the host-virus interface: mechanistic roles in viral RNA translation, replication, and immune modulation.","authors":"Kajal, Achyut Pandey, Rajesh Yadav, Rishikesh Shukla, Shruti Mishra","doi":"10.1007/s11033-026-12713-x","DOIUrl":"https://doi.org/10.1007/s11033-026-12713-x","url":null,"abstract":"<p><p>Viruses require the involvement of host RNA binding proteins for completion of important steps of their life cycle. Polypyrimidine tract binding protein 1 (PTBP1) is an RNA-binding protein found ubiquitously which performs important regulatory functions like alternative splicing, RNA stability, RNA localization, and translation by virtue of its four RRMs and shuttling between nucleus and cytoplasm. There is increasing evidence showing that many viruses make use of such regulatory roles of PTBP1 to facilitate their gene expression and replication. This review describes the existing mechanistic knowledge about the PTBP1 functions during viral infection, paying attention to the role of PTBP1 in viral RNA translation, viral RNA genome replication, and regulation of host antiviral response. Special attention is paid to the regulation by PTBP1 of IRES-dependent translation of enteroviruses and hepatitis C virus, as well as to the PTBP1 contribution to RNA stabilization, long-distance RNA interactions, and genome cyclization of flaviviruses such as dengue virus and Japanese encephalitis virus. Recent data on the PTBP1 function in coronavirus RNA metabolism are discussed as well. Furthermore, the role of PTBP1 in being both proviral and antiviral is reviewed in terms of innate immunity signalling pathways, stress granule biology, and virus-host interaction. Finally, we will explore the possibility of PTBP1 being used as a host-directed antiviral drug target despite the hurdles in doing so considering its multifunctionality as an essential cellular RNA-binding protein.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891351","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":"Hepatoprotective effects of cinnamic acid against carbon tetrachloride-induced liver injury in a mouse model.","authors":"Samira Nomiri, Reyhaneh Taebi, Yaser Mohammadi, Tooba Yousefi, Fatemeh Asgari, Farzaneh Yazdanimoghaddam, Nafiseh Mortazavi, Abdollah Amini","doi":"10.1007/s11033-026-12643-8","DOIUrl":"https://doi.org/10.1007/s11033-026-12643-8","url":null,"abstract":"<p><strong>Background: </strong>Cinnamic acid (CA), a natural phenolic compound with antioxidant and anti-inflammatory properties, has recently attracted attention for its potential protective effects on liver function. This study aimed to evaluate the hepatoprotective effects of CA against carbon tetrachloride (CCl₄)-induced toxicity in mice.</p><p><strong>Methods: </strong>Thirty NMRI mice were randomly divided into five groups: control, CCl₄, and three groups treated with CA (50, 100, and 200 mg/kg). CA was administered orally for seven days prior to CCl₄ injection. Serum biochemical parameters and total antioxidant capacity (TAC) were measured. Gene expression levels of Nrf2, Foxo3, IL-6, and TNF-α, as well as liver histology, were also assessed.</p><p><strong>Results: </strong>CCl₄ exposure markedly elevated hepatic enzymes, bilirubin, urea, and C-reactive protein (CRP) levels while reducing albumin and total protein concentrations. Pretreatment with CA improved several of these parameters, particularly at higher doses (100-200 mg/kg). Although CA treatment did not significantly restore TAC levels, higher CA doses (100-200 mg/kg) upregulated Nrf2 and Foxo3, suggesting activation of antioxidant-related signaling pathways, and downregulated IL-6 and TNF-α expression, indicating reduced inflammatory marker expression. TNF-α. Histopathological analysis confirmed these biochemical findings, showing reduced necrosis and inflammation in CA-treated mice.</p><p><strong>Conclusion: </strong>Cinnamic acid may exert hepatoprotective effects against CCl₄-induced liver injury, with secondary favorable effects on renal biochemical markers of CCl₄-induced systemic toxicity, by modulating oxidative and inflammatory pathways. Its association with increased Nrf2 and Foxo3 expression and reduced inflammatory mediator expression supports further investigation of CA as a potential hepatoprotective compound.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892178","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}