Biochemical and biophysical research communications最新文献

{"title":"5-Fluorouracil induces ferroptosis in breast cancer cells via targeting SLC7A11","authors":"Guojie Ji ,&nbsp;Wenzheng Yuan ,&nbsp;Xiaoyi Wang,&nbsp;Wenmi Li,&nbsp;Zhibin Sun,&nbsp;Ziyu Wei,&nbsp;Liuyang Zhou,&nbsp;Huanhuan Hu","doi":"10.1016/j.bbrc.2025.151972","DOIUrl":"10.1016/j.bbrc.2025.151972","url":null,"abstract":"<div><div>Breast cancer (BC) is one of the major causes of cancer mortality worldwide among women. 5-Fluorouracil (5-FU) is a widely used chemotherapy drug to treat breast cancer, which is unclear that the mechanism of inhibiting BC. Ferroptosis is a mode of programmed cell death determined by iron-dependent lipid peroxidation. The aim of the study was to investigate whether ferroptosis is involved in 5-FU-induced BC cell injury. In the current study, we found that iron metabolism and SLC7A11/GPX4 signaling may play a key role in cell death of BC induced by 5-FU in vitro. In vitro experiments, we found that 5-FU exposure significantly increased the levels of iron and reactive oxygen species (ROS) in MCF-7 and MDA-MB-231 cells. Furthermore, ferrostatin-1, the ferroptosis inhibitor, inhibited cell death induced by 5-FU. Subsequent western blotting, qRT-PCR, and measurement of various kits, fluorescence staining as well as cellular thermal shift assay, confirmed the results that 5-FU induces ferroptosis by targeting SLC7A11 in BC cells. In conclusion, the results in our study reveals that 5-FU exposure leads to ferroptosis in BC cells via targeting inhibition of SLC7A11/GPX4 signaling pathway, which offers novel insight in pharmacodynamic effect and mechanism of 5-FU in therapeutic avenues of BC.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"770 ","pages":"Article 151972"},"PeriodicalIF":2.5,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"S-ketamine ameliorates post-stroke depression in mice via attenuation of neuroinflammation, synaptic restoration, and BDNF pathway activation","authors":"Jiaxin Tian ,&nbsp;Yanhong Xie ,&nbsp;Sen Ye ,&nbsp;Yongfeng Hu ,&nbsp;Jiaxin Feng ,&nbsp;Yi Li ,&nbsp;Zhongze Lou ,&nbsp;Liemin Ruan ,&nbsp;Zhengchun Wang","doi":"10.1016/j.bbrc.2025.151965","DOIUrl":"10.1016/j.bbrc.2025.151965","url":null,"abstract":"<div><div>The available therapeutic options for post-stroke depression patients are limited. Although SSRIs are the most commonly prescribed antidepressants, their slow onset of action and the higher risk of adverse effects or contraindications have led to an urgent need to develop fast-acting and highly specific antidepressants tailored to the needs of PSD patients. Therefore, ketamine has drawn attention. While ketamine has been shown to exert rapid antidepressant effects in numerous studies, whether it can ameliorate PSD remains unclear, and the molecular and cellular mechanisms underlying its therapeutic action in PSD are largely elusive. In this study, we used a PSD preclinical model induced by photothrombosis and chronic restraint stress to investigate the effects of <em>S</em>-ketamine. The present study demonstrates that a single acute intraperitoneal injection of 10 mg/kg <em>S</em>-ketamine on the first day after PSD significantly alleviates depressive-like behaviours in PSD mice. In addition, this improvement was maintained for at least five consecutive days. Mechanistically, <em>S</em>-ketamine reduced pro-inflammatory cytokines in the medial prefrontal cortex (mPFC), mitigated synaptic damage (evidenced by increased dendritic spine density, SYP, and PSD-95 expression). Furthermore, <em>S</em>-ketamine treatment upregulated the expression of brain-derived neurotrophic factor (BDNF), tropomyosin related kinase B (TrkB), phosphorylated serine/threonine-specific protein kinase B (p-Akt), phosphorylated extracellular signal–regulated kinase (p-Erk), phosphorylated calcium/calmodulin-dependent protein kinase II (p-CaMKII), and phosphorylated cAMP response element binding protein (p-CREB). Overall, <em>S</em>-ketamine shows promise for PSD treatment through its anti-inflammatory, synaptic enhancing, and BDNF pathway modulating effects. This research enhances our understanding of the pathological mechanisms underlying PSD and provides new therapeutic insights for its treatment.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"769 ","pages":"Article 151965"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nano encapsulated polymeric Scopoletin suppresses the progression of colorectal cancer by regulating cytokines and inflammatory mediators in AOM/DSS murine model","authors":"Kunnathur Murugesan Sakthivel ,&nbsp;Rajan Radha Rasmi ,&nbsp;Loganathan Chandramani Priya Dharshini ,&nbsp;Kalavathi Murugan Kumar ,&nbsp;Venugopal Vinod Prabhu ,&nbsp;Balasubramanian Ramesh","doi":"10.1016/j.bbrc.2025.151973","DOIUrl":"10.1016/j.bbrc.2025.151973","url":null,"abstract":"<div><div>Scopoletin (6-methoxy-7-hydroxycoumarin) belongs to the family of coumarins with numerous pharmacological benefits. The present study deals with examining the efficacy of Nanoencapsulated polymeric Scopoletin (NEP-Sc) in murine colon cancer model. Male Balb/c mice were supplemented with NEP-Sc (2.5 and 5 mg/kg b.w.) and 5-fluorouracil (25 mg/kg b.w.) for 10 days consecutively post-induction of colon cancer. Colon polyps and morphology were assessed using a macroscopical inspection, and their score establishes the ameliorative effect of NEP-Sc. Body weight, diarrhoea score, and spleen weight were also measured. The antioxidant status of the mucosal levels of glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (LPO) and nitric oxide (NO) were evaluated. The β-catenin and Ki-67 levels were analyzed through immunohistochemistry analysis to assess the inflammatory response. ELISA-based analysis was used to measure IL-4, IL-6, IL-10, TNF-alpha, IFN-gamma, and VEGF levels. All the aforementioned parameters were mitigated in AOM/DSS-triggered colon cancer in mice treated with NEP-Sc. Nanoencapsulated polymeric Scopoletin offered protection against AOM/DSS-induced colon cancer in mice. To sum up, our research findings suggest that NEP-Sc may act as a promising candidate for treating colon-associated cancer.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"769 ","pages":"Article 151973"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143931364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Connectivity-map unveils Gemcitabine's efficacy in overcoming nelarabine resistance in T-cell acute lymphoblastic leukemia","authors":"Ximei Wu ,&nbsp;Chunxu Lin ,&nbsp;Hui Wang ,&nbsp;Jingjing Gao ,&nbsp;Suchang chen ,&nbsp;Zitao Zhou ,&nbsp;Luyong Zhang ,&nbsp;Bing Liu ,&nbsp;Min Wei","doi":"10.1016/j.bbrc.2025.151971","DOIUrl":"10.1016/j.bbrc.2025.151971","url":null,"abstract":"<div><div>Resistance to Nelarabine, the primary FDA-approved therapy for relapsed/refractory T-cell acute lymphoblastic leukemia (T-ALL), is a major obstacle in this high-risk pediatric malignancy. To identify alternative therapies, we have developed two nelarabine-resistant T-ALL cell models and utilized the Connectivity Map (CMap) database to screen for compounds reversing resistance-associated expression profiles., Among the inhibitors screened, gemcitabine emerged as a lead candidate by inhibiting cell proliferation, inducing apoptosis, and suppressing DNA replication in resistant T-ALL cells. RNA sequencing revealed global transcriptomic changes in cells treated with gemcitabine, which were further validated by qRT-PCR. Critically, gemcitabine effectively controlled bone marrow tumor growth in an NSG mouse model with good tolerability. These findings highlight the potential of gemcitabine as a promising therapeutic strategy to overcome nelarabine-resistance in T-ALL.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"769 ","pages":"Article 151971"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electrophysiological and molecular docking analysis of 1,8-Cineole's effects on potassium currents in mouse DRG neurons","authors":"Ana Beatriz Gomes ,&nbsp;Lucas Almeida Vaz ,&nbsp;Jeremias Martins Gonçalves ,&nbsp;José Ednésio da Cruz Freire ,&nbsp;Kerly Shamyra da Silva-Alves ,&nbsp;Humberto Cavalcante Joca ,&nbsp;Bianca de Sousa Barbosa-Ferreira ,&nbsp;Andrelina Noronha Coelho-de-Souza ,&nbsp;José Henrique Leal-Cardoso ,&nbsp;Francisco Walber Ferreira-da-Silva","doi":"10.1016/j.bbrc.2025.151968","DOIUrl":"10.1016/j.bbrc.2025.151968","url":null,"abstract":"<div><div>1,8-cineole (CIN) is a monoterpene widely used in traditional medicine, as it promotes biological and pharmacological effects, including the inhibition of neuronal excitability. This inhibition might be due to ion channel blockade, as reported for voltage-dependent Na⁺ and Ca²⁺ channels. However, voltage-dependent K⁺ channels (K_v) are also relevant proteins in neuronal excitability. Thus, this study investigated the effects of CIN on potassium current (I_K+) in dissociated neurons from mouse dorsal root ganglia (DRG) using electrophysiological and molecular docking approaches. The whole-cell patch-clamp technique recorded I_K+ in voltage-clamp mode. Other experiments recorded action potentials (APs) in the current-clamp mode, and molecular docking used specific software (AutoDock Vina, LigPlot⁺, PyMol). Consequently, CIN achieved a partial concentration-dependent inhibition of I_K+. CIN at 3.0 and 6.0 mM showed similar blockade values of ∼50 % of peak and sustained I_K+. IV plots from cells exposed to 3.0 mM CIN shifted by ∼15 mV toward negative values in the G/G_max curve of sustained I_K+. Peak I_K + had no significant shift. Molecular docking simulations demonstrated that CIN interacts with the binding pockets of K_v2.1 and K_v3.4 channels with ΔG values of −4.7 kcal.mol⁻¹ and −2.0 kcal.mol⁻¹ interaction energy, respectively. This study also investigated 3 mM CIN effects on neuronal excitability. CIN blocked APs in two of eight neurons and altered several electrophysiological parameters related to excitability in the remaining six neurons. These parameters included AP amplitude, AP maximum rise slope, and AP time-to-peak without changes in resting membrane potential. This study concluded that CIN blocks total I_K+ and interacts with K⁺ channels. Also, the changes in neuronal excitability might be due to CIN effects on K⁺ channels, working through a mechanism independent of resting membrane potential.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"773 ","pages":"Article 151968"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144139651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between sleep disturbance and metabolic dysfunctions in adipose tissue: Insights into melatonin's role","authors":"Mishthi Ratwani ,&nbsp;Shradha Bisht ,&nbsp;Swati Prakash","doi":"10.1016/j.bbrc.2025.151978","DOIUrl":"10.1016/j.bbrc.2025.151978","url":null,"abstract":"<div><div>The increased prevalence of sleep disturbances in modern society is frequently linked to various metabolic disorders, including insulin resistance, obesity, hypertension, fatty liver disease, and cardiometabolic complications. Melatonin, a pineal gland-secreted neurohormone, plays a pivotal role in maintaining the circadian rhythm. It is involved in regulating adipose tissue development, lipid accumulation, browning of white adipose tissue, and activation of brown adipose tissue. The adipose tissue is a dynamic endocrine organ that secretes hormones and cytokines. Recent research has highlighted the significant role of melatonin in the modulation of lipid metabolism, adipogenesis, and thermogenesis in adipose tissues. Circadian rhythms are important in synchronizing metabolic functions with environmental cues, such as light and dark, feeding-fasting states, etc. Irregular sleep patterns, shift work, and exposure to artificial light at night disrupt these rhythms, affecting circadian regulation and compromising metabolic health. Melatonin imbalance due to sleep disturbances results in metabolic dysfunction, increased fat storage, and adipose tissue inflammation. As circadian rhythm and melatonin are both related, a change in circadian rhythm affects the physiology of adipose tissues thereby precipitating metabolic complications through melatonin signaling. This study attempted to understand the mechanisms by which melatonin influences adipose tissue activity, highlighting the role of circadian rhythms in this process. This will enable the development of melatonin-based therapies to mitigate the adverse effects of chronobiological disturbances on the physiology of adipose tissue. Understanding these interactions will provide novel insights for combating obesity and related metabolic conditions.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"770 ","pages":"Article 151978"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143950482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect and mechanism of areca nut in ovarian cancer were investigated based on network pharmacology, molecular docking, and in vitro experiments","authors":"Shumin Xu ,&nbsp;Qinran Zhu ,&nbsp;Jian Zhang ,&nbsp;Xin Li ,&nbsp;Meng Liang ,&nbsp;Junpei Sun","doi":"10.1016/j.bbrc.2025.151943","DOIUrl":"10.1016/j.bbrc.2025.151943","url":null,"abstract":"<div><h3>Background</h3><div>Ovarian cancer ranks as the leading cause of death among gynecological malignancies[1, 2]. Areca nut has demonstrated notable antitumor activity, yet its underlying mechanism remains incompletely understood.</div></div><div><h3>Objective</h3><div>To explore the potential of areca nut - derived active ingredients in regulating ovarian cancer progression via the PTEN/AKT1 signaling axis.</div></div><div><h3>Methods</h3><div>Targets related to areca nut were screened from the TCMSP database, while ovarian - cancer - associated targets were retrieved from GeneCards and DisGeNET databases. Intersection targets were identified using Venn analysis. Core pathways were annotated through enrichment analysis with Metascape and DAVID databases. Molecular docking was performed to validate the binding energy intensity between areca nut active ingredients and their corresponding receptors. In addition, the effect of arecoline on ovarian cancer cells was investigated in vitro.</div></div><div><h3>Results</h3><div>A total of 50 common targets were identified from 139 areca nut - related targets and 1914 ovarian cancer - associated targets. Pathway enrichment analysis revealed significant enrichment of the PI3K/AKT pathway. The core targets, <em>PTEN</em> (−5.3 kJ/mol) and <em>AKT1</em> (−5.4 kJ/mol), exhibited strong binding to the active components of areca nut. Moreover, arecoline inhibited the proliferation and induced apoptosis in ovarian cancer cells.</div></div><div><h3>Conclusion</h3><div>In conclusion, this study provides a solid scientific basis for exploring the action mechanism of areca nut.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"771 ","pages":"Article 151943"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144089200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of DDIT3 in modulating proliferation and tamoxifen resistance in luminal A subtype breast cancer through the DDIT3-IRF1 axis","authors":"Guoqing Huang,&nbsp;Dandan Wang,&nbsp;Jiaying Xue","doi":"10.1016/j.bbrc.2025.151922","DOIUrl":"10.1016/j.bbrc.2025.151922","url":null,"abstract":"<div><h3>Background</h3><div>This study investigates the role of DNA Damage Inducible Transcript 3 (DDIT3) in luminal A subtype breast cancer (LABC). DDIT3, a transcription factor linked to various stress responses, has been implicated in tumorigenesis, yet its specific contributions to LABC biology remain poorly understood.</div></div><div><h3>Methods</h3><div>To elucidate these functions, we utilized bioinformatics analyses, including data from TCGA and Kaplan-Meier databases. Furthermore, we performed siRNA-mediated knockdown and overexpression experiments in MCF-7 and T47D cells to assess DDIT3's functional impact on cell proliferation, drug resistance, etc. RNA sequencing analysis identified differentially expressed genes (DEGs) associated with DDIT3 manipulation, and pinpointing the crucial downstream target with rescue experiment.</div></div><div><h3>Results</h3><div>Compared to normal breast tissue, DDIT3 is lowly expressed in LABC, and LABC patients with low DDIT3 expression have a lower survival rate, indicating relatively poor prognosis. Furthermore, DDIT3 negatively regulates the proliferation of LABC cells, also negatively correlated with the sensitivity of TAM. RNA-seq result and rescue experiment identified the interferon regulatory factor 1 (IRF1) as a crucial downstream target of DDIT3 to regulating LABC cell proliferation and tamoxifen (TAM) resistance.</div></div><div><h3>Conclusions</h3><div>DDIT3 is negatively correlated with poor prognosis in LABC patients. And DDIT3 may negatively regulate the proliferation and TAM sensitivity in LABC cells through the DDIT3-IRF1 axis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"769 ","pages":"Article 151922"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Delivery of cancer cell-derived extracellular vesicles modulates the morphology and gene expression of Barrett esophagus and duodenal organoids (Article)","authors":"Rong Yan ,&nbsp;Xiquan Ke ,&nbsp;Yulan Cheng ,&nbsp;Xi Liu ,&nbsp;Zhixiong Wang ,&nbsp;Stephen J. Meltzer","doi":"10.1016/j.bbrc.2025.151976","DOIUrl":"10.1016/j.bbrc.2025.151976","url":null,"abstract":"<div><div>Extracellular vesicles (EVs) facilitate intercellular communication, especially in the signaling mechanisms employed by tumor cells to influence both local and distant cells and tissues. This study investigated the impact of cancer cell-derived EVs (CEVs) on patient-derived organoids. Co-culture experiments examined the morphology, growth, proliferation, and cancer-related gene/miRNA expression in Barrett's esophagus (BE) and duodenal organoids. Our results indicate that CEVs promoted organoid proliferation, increased cancer-related mRNA/miRNA expression, and induced phenotypic changes. Artificial modulation of specific oncomiRNAs in CEVs—such as miR-21 and miR-210, influenced CEV-mediated effects on co-cultured organoid growth. These findings align with EV-mediated transformations in benign organoid models, providing a valuable tool to study EV-associated miRNAs/proteins in gastrointestinal preneoplastic/neoplastic conditions and potentially other organs. This lays a foundation for future research on cancer cell-microenvironment interactions and EV roles in tumorigenesis/metastasis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"769 ","pages":"Article 151976"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143928182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alleviation of fibrosis and oxidative stress in pressure overload-induced cardiac remodeling and heart failure via SIRT3 activation by colchicine","authors":"Mengze Wu ,&nbsp;Guodong Chen ,&nbsp;Yuce Peng,&nbsp;Suxin Luo","doi":"10.1016/j.bbrc.2025.151957","DOIUrl":"10.1016/j.bbrc.2025.151957","url":null,"abstract":"<div><div>Heart failure (HF) is the end stage of many cardiovascular diseases, which is often associated with myocardial hypertrophy and cardiac remodeling. Among them, pressure overload-induced myocardial injury is one of the most common causes of heart failure. Colchicine, a drug widely used in the treatment of inflammatory diseases, has recently been found to significantly reduce the risk of cardiovascular events in patients with coronary artery disease and atrial fibrillation. However, the specific mechanism of colchicine has not been fully elucidated. We used the transverse aortic constriction (TAC) model to simulate cardiac pressure overload in mice. We found that colchicine attenuated TAC-induced heart failure and alleviated cardiac oxidative stress and fibrosis. To explore the specific molecular mechanism, we treated primary cardiac fibroblasts (CFs) and HL-1 with Ang Ⅱ in vitro to simulate the occurrence of TAC model. We found that colchicine induced SIRT3 activation and alleviated myocardial oxidative stress and cadiac fibrosis. Additionally, the SIRT3-selective agonist HKL exerts similar effects to colchicine, whereas the SIRT3-selective inhibitor 3-TYP partially reverses the therapeutic effects of colchicine. Our findings suggest that colchicine reduced cardiac oxidative stress and fibrosis by activating SIRT3, which in turn alleviated the progression of pressure overload-induced heart failure.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"770 ","pages":"Article 151957"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143941411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}