Redox Report最新文献

{"title":"The estrogen-progestogen-oxidative stress network in uterine fibroids: mechanistic insights and therapeutic opportunities.","authors":"Siyu Wang, Wanhui You, Danni Ding, Fangyuan Liu, Fengjuan Han, Liping Tang","doi":"10.1080/13510002.2026.2622747","DOIUrl":"10.1080/13510002.2026.2622747","url":null,"abstract":"<p><p>Uterine fibroids are benign tumors with high incidence and recurrence rates that still pose significant treatment challenges. Traditionally, it has been believed that estrogen and progesterone primarily drive the development and progression of uterine fibroids. Recent studies have revealed that hormonal imbalance can affect reactive oxygen species production and trigger a significant oxidative stress (OS) state. The OS status in uterine fibroids can further amplify the pathological effects caused by hormonal imbalance. This suggests that estrogen, progesterone, and OS may interact to form an estrogen-progesterone-oxidative stress (E-P-OS) network, collectively promoting the progression of uterine fibroids. This network model provides a theoretical basis for the high recurrence rates following hormone monotherapy or surgery. Therefore, we reviewed the molecular mechanisms underlying hormone-OS interactions within the E-P-OS network and elucidated its pathological effects in promoting uterine fibroid progression. The integrated perspective lays the theoretical foundation for developing novel therapies that simultaneously block hormone signaling and counteract oxidative damage. Additionally, we summarized current clinical strategies for hormone therapy and antioxidant treatment, identified potential combination therapy approaches, and explored key challenges in their clinical translation. This aims to provide new directions and evidence for advancing the precision treatment of uterine fibroids.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2622747"},"PeriodicalIF":6.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12879505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146119694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DRP1 depletion protects NK cells from hypoxia-induced dysfunction.","authors":"Tias Verhezen, Astrid Van Den Eynde, Peter Verstraelen, Laura Gehrcken, Gabriele Palmiotto, Ho Wa Lau, Winnok H De Vos, Sanne Van Der Heijden, Louize Brants, Jöran Melis, Jonas Van Audenaerde, Felicia Rodrigues Fortes, Maxim Le Compte, Geert Roeyen, Hans Prenen, Diana Campillo-Davo, Eva Lion, Rafael J Argüello, Steven Van Laere, Filip Lardon, Christophe Deben, An Wouters, Evelien Smits, Jorrit De Waele","doi":"10.1080/13510002.2026.2626181","DOIUrl":"10.1080/13510002.2026.2626181","url":null,"abstract":"<p><strong>Objectives: </strong>The efficacy of cellular therapies has been disappointing in solid tumors. A major barrier that contributes to the low success rate, is hypoxia within the tumor microenvironment. In this study, we investigated the influence of hypoxia on natural killer (NK) cell function and to evaluated a strategy to restore their activity in hypoxia.</p><p><strong>Methods: </strong>Unarmed or CAR NK cells were placed in normoxia (21% O₂) or hypoxia (1% O₂) prior to experimental readouts. Mitochondrial content and morphology were assessed by confocal microscopy, membrane potential and reactive oxygen species (ROS) by flow cytometry, and global transcriptional changes by RNA sequencing. Cytotoxicity was evaluated against tumor cell lines and patient-derived cancer organoids, which were characterized by RNA sequencing. DRP1 function was inhibited pharmacologically or through CRISPR-Cas9-mediated knockout.</p><p><strong>Results: </strong>Hypoxia reduced NK cell mitochondrial content and membrane potential, while increasing mitochondrial ROS and inducing broad transcriptional changes in stress response pathways. Their cytotoxic activity was drastically impaired, which could not be prevented by CD70-CAR-IL-15 engineering. Pharmacological inhibition of DRP1 restored mitochondrial content and cytotoxic function. To confirm the role of DRP1, CRISPR-Cas9-mediated <i>DRP1</i> knockout (KO) NK cells preserved mitochondrial load and membrane potential under hypoxia, and DRP1^KO CAR NK cells retained cytotoxic activity under hypoxic conditions against cancer cell lines. Patient microtumor models with distinct transcriptomic profiles exhibited divergent responses to DRP1^WT and DRP1^KO CAR NK cells.</p><p><strong>Conclusion: </strong>These findings indicate that DRP1 inactivation supports NK cell function in hypoxia and metabolic engineering may enhance CAR-NK efficacy in solid tumors.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2626181"},"PeriodicalIF":6.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146220804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artesunate ameliorates experimental autoimmune uveitis by inhibiting the LCN2-STAT3 axis and suppressing microglial activation.","authors":"Jingsai Gu, Qinyun Xia, Pingping Huang, Yilin Yuan, He Ren, Dihao Hua, Zhen Chen","doi":"10.1080/13510002.2026.2627096","DOIUrl":"10.1080/13510002.2026.2627096","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the efficacy and underlying molecular mechanisms of artesunate (ART) in experimental autoimmune uveitis (EAU).</p><p><strong>Methods: </strong>An EAU mouse model was established and treated with ART via oral gavage. Disease severity was assessed by clinical scoring and retinal histology. SPR analysis examined ART binding to LCN2 and STAT3. Immunofluorescence co-staining was conducted to evaluate the expression and co-localization of LCN2 with microglia in retinal tissues. Western blot analysis was performed to measure protein levels of STAT3, LCN2, SLC7A11, FTH1, GPX4, IL-6, IL-1β, IL17A and TNF-α. In vitro, BV2 microglial cells were used, and LCN2 was knocked down with siRNA. Inflammatory cytokine concentrations in retina and BV2 cell culture supernatants were assessed through ELISA.</p><p><strong>Results: </strong>ART treatment significantly improved clinical and histopathological scores in EAU mice and exhibited moderate binding affinity for LCN2 and STAT3. It suppressed microglial activation and downregulated the expression of LCN2 and STAT3, along with the release of IL-6, IL-1β, IL17A and TNF-α. In BV2 microglial cells, ART decreased LCN2 expression and attenuated proinflammatory cytokine secretion.</p><p><strong>Conclusions: </strong>Artesunate attenuates EAU by inhibiting the LCN2-STAT3 axis and suppressing the activation of microglial and Th17 cells.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2627096"},"PeriodicalIF":6.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12903941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146166614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"XFM and HERFD-XAS studies of selenium in tissues and whole blood from mice supplemented with potentially therapeutic selenocompounds.","authors":"Ani T Baker, Tamara Ortiz-Cerda, Kangzhe Xie, Jordan Hunter, Iliya Dragutinovic, Jonathan C Morris, Linda I Vogt, Graham N George, Dimosthenis Sokaras, Daryl L Howard, Paul K Witting, Hugh H Harris","doi":"10.1080/13510002.2026.2626151","DOIUrl":"10.1080/13510002.2026.2626151","url":null,"abstract":"<p><strong>Background: </strong>Selenium nanoparticles (SeNPs) and selenoneine (SeN) are prospective nutritional supplements and therapeutic agents postulated to counteract Se deficiency and alleviate oxidative stress induced by various pathological conditions.</p><p><strong>Methods: </strong>X-ray fluorescence microscopy (XFM) and high energy resolution fluorescence detected X-ray absorption spectroscopy (HERFD-XAS) investigated Se distribution and speciation in mice fed supranutritional doses of SeNPs (10 mg Se/kg in feed) and SeN (5 mg Se/kg in feed).</p><p><strong>Results: </strong>Mice fed control and SeNP diets showed equivalent Se distributions in the liver and testes, however, Se concentrations were elevated in the renal tubules of mice supplemented with SeNPs. Negligible differences in the composition of selenospecies were detected in tissues from mice fed SeNPs and control diets. Mice supplemented with SeN exhibited significant elevations in Se across all analysed tissues. Se Kα₁ HERFD-XAS data revealed reduced SeN as the predominant selenospecies in tissues and blood from mice fed the SeN diet. Characterisation of the SeN-enriched feed showed that SeN was initially present in both the oxidised dimer and reduced monomer forms.</p><p><strong>Conclusion: </strong>These results support the hypothesised <i>in vivo</i> reduction of SeN and subsequent bioaccumulation in the blood and various tissues. The present findings highlight marked differences in the bioavailability and utilisation of these purported therapeutic selenocompounds.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2626151"},"PeriodicalIF":6.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12912245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146207564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MSC-mediated mitochondrial transfer promotes metabolic reprograming in endothelial cells and vascular regeneration in ARDS.","authors":"Jinlong Wang, Shanshan Meng, Yixuan Chen, Haofei Wang, Wenhan Hu, Shuai Liu, Lili Huang, Jingyuan Xu, Qing Li, Xiaojing Wu, Wei Huang, Yingzi Huang","doi":"10.1080/13510002.2025.2474897","DOIUrl":"10.1080/13510002.2025.2474897","url":null,"abstract":"<p><strong>Background: </strong>Mesenchymal stem cells (MSCs) are a potential therapy for acute respiratory distress syndrome (ARDS), but their mechanisms in repairing mitochondrial damage in ARDS endothelial cells remain unclear.</p><p><strong>Methods: </strong>We first examined MSCs' mitochondrial transfer ability and mechanisms to mouse pulmonary microvascular endothelial cells (MPMECs) in ARDS. Then, we investigated how MSC-mediated mitochondrial transfer affects the repair of endothelial damage. Finally, we elucidated the mechanisms by which MSC-mediated mitochondrial transfer promotes vascular regeneration.</p><p><strong>Results: </strong>Compared to mitochondrial-damaged MSCs, normal MSCs showed a significantly higher mitochondrial transfer rate to MPMECs, with increases of 41.68% in vitro (<i>P</i> < 0.0001) and 10.50% in vivo (<i>P</i> = 0.0005). Furthermore, MSC-mediated mitochondrial transfer significantly reduced reactive oxygen species (<i>P</i> < 0.05) and promoted proliferation (<i>P</i> < 0.0001) in MPMECs. Finally, MSC-mediated mitochondrial transfer significantly increased the activity of the tricarboxylic acid (TCA) cycle (MD of CS mRNA: 23.76, <i>P</i> = 0.032), and further enhanced fatty acid synthesis (MD of FAS mRNA: 6.67, <i>P</i> = 0.0001), leading to a 6.7-fold increase in vascular endothelial growth factor release from MPMECs and promoted vascular regeneration in ARDS.</p><p><strong>Conclusion: </strong>MSC-mediated mitochondrial transfer to MPMECs activates the TCA cycle and fatty acid synthesis, promoting endothelial proliferation and pro-angiogenic factor release, thereby enhancing vascular regeneration in ARDS.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2474897"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rotenone inhibited osteosarcoma metastasis by modulating ZO-2 expression and location via the ROS/Ca²⁺/AMPK pathway.","authors":"Xiang Ma, Zhen Li, Hengwei Ma, Kun Jiang, Bao Chen, Weiquan Wang, Ziqiang Zhu, Jianqiang Wang, Zuozhang Yang, Wang Yunqing, Suwei Dong","doi":"10.1080/13510002.2025.2493556","DOIUrl":"https://doi.org/10.1080/13510002.2025.2493556","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary metastases in osteosarcoma (OS) are associated with a poor prognosis. Rotenone has shown anti-cancer activity. However, its effects on metastasis and the underlying mechanisms remain unknown. This study investigated the potential use of Rotenone for OS treatment.</p><p><strong>Methods: </strong>The effect of Rotenone and ROS/Ca²⁺/AMPK/ZO-2 pathway on metastasis and EMT was evaluated by Western blot, Transwell and Wound healing. Flow cytometer was employed to measure the intracellular Ros and Ca²⁺ levels. The subcellular location of ZO-2 was detected by IF, interaction between AMPK and ZO-2 were examined by Co-IP. Then, subcutaneous tumor and metastasis models were used to evaluate the function of Rotenone in OS metastasis.</p><p><strong>Results: </strong>Rotenone-induced ROS led to increased intracellular Ca²⁺, which promoted the EMT of OS cells through activation of AMPK and ZO-2 nuclear translocation. Inhibition of ROS production decreased intracellular Ca²⁺, restraining AMPK activity. Knock-down of ZO-2 significantly suppressed the anti-metastasis effects of Rotenone in OS cells. Moreover, Rotenone elevated p-AMPK and ZO-2 expression but inhibited EMT and lung metastasis in <i>vivo</i>.<b>Conclusion</b> These results provide evidence supporting an anti-metastatic effect of Rotenone. These findings support the use of Rotenone in the prevention of OS metastasis.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2493556"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HIF1A/BNIP3 pathway affects ferroptosis in sepsis-induced cardiomyopathy through binding to BCL-2.","authors":"Xiaoyue Wang, Jinze Li, Yixin Zhang, Ming Huang, Pengqiang Yang, Tianwen Huang, Qinghong Cheng","doi":"10.1080/13510002.2025.2544412","DOIUrl":"10.1080/13510002.2025.2544412","url":null,"abstract":"<p><strong>Background: </strong>Sepsis-induced cardiomyopathy (SIC) involves ferroptosis, an iron-dependent cell death. Hypoxia-inducible factor-1α (HIF-1α) regulates autophagy and apoptosis, but its role in ferroptosis remains unclear. This study investigates the interaction between the HIF1A/BNIP3 signaling pathway and the ferroptosis axis, SLC7A11/GPX4, in septic myocardial injury.</p><p><strong>Methods: </strong>A rat model of septic myocardial injury was created via cecal ligation and puncture (CLP), with an in vitro model using lipopolysaccharide (LPS)-treated H9c2 cardiomyocytes. Groups: sham, CLP, CLP + solvent, CLP + HIF1A inhibitor (LW6), CLP + ferroptosis inhibitor (Fer-1), and CLP + LW6 + Fer-1. Cardiac function, histopathological changes, and biomarkers (myocardial injury/inflammation/ferroptosis) were measured. In vitro, H9c2 cells were treated with LPS, LW6, or fenbendazole (FZ) and transfected with BNIP3 shRNA. Various assays were used to evaluate cell viability, ROS levels, and protein interactions.</p><p><strong>Results: </strong>(1) HIF1A/BNIP3 activation aggravated septic myocardial injury and ferroptosis; inhibition reversed this. (2) BNIP3 knockdown alleviated LPS-induced injury and ferroptosis in H9c2 cells. (3) BNIP3 and BECN1 competed for BCL-2 binding, modulating ferroptosis-related signaling.</p><p><strong>Conclusion: </strong>BCL-2 links the HIF1A/BNIP3 and BECN1/SLC7A11/GPX4 pathways, offering insights into septic myocardial injury mechanisms and potential therapeutic targets.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2544412"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12337741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144804668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Varespladib attenuates <i>Naja atra</i>-induced acute liver injury via reversing Nrf2 signaling-mediated ferroptosis and mitochondrial dysfunction.","authors":"Jiahao Liu, Linfeng Wang, Mengxia Xie, Wenjie Zhao, Jiaqi Sun, Yuji Jin, Meiling Liu, Jianqi Zhao, Lixia Cheng, Cheng Wen, Xiaowen Bi, Chunhong Huang","doi":"10.1080/13510002.2025.2507557","DOIUrl":"10.1080/13510002.2025.2507557","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the protective effects of varespladib against <i>Naja atra</i>-induced acute liver injury (ALI) and to elucidate the toxic mechanism of snake venom phospholipase A₂ (SVPLA₂)-induced hepatic oxidative stress, with a particular focus on the role of Nrf2 signaling and its downstream pathways.<b>Methods:</b> A combination of in vivo and in vitro models of <i>N. atra</i> envenomation was employed to assess liver injury, oxidative stress, and mitochondrial dysfunction. The interaction between SVPLA₂ and Nrf2 was analyzed, and the effects of varespladib treatment on these processes were evaluated using histological analysis, biochemical assays, and molecular techniques targeting oxidative stress, ferroptosis, mitophagy, and apoptosis.<b>Results:</b> Varespladib significantly alleviated <i>N. atra</i>-induced ALI. SVPLA₂ was found to directly bind to Nrf2, leading to severe oxidative stress. This oxidative stress initiated a cascade involving Nrf2-mediated ferroptosis, mitochondrial dysfunction, excessive mitophagy, and mitochondria-dependent apoptosis. Treatment with varespladib effectively reversed these pathological events by inhibiting SVPLA₂ activity.<b>Conclusion:</b> Varespladib shows strong therapeutic potential for <i>N. atra</i> envenomation by targeting SVPLA₂. Nrf2 was identified as a direct toxic target of SVPLA₂, and Nrf2-mediated ferroptosis and mitochondrial dysfunction were key mechanisms underlying SVPLA₂-induced hepatic injury.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2507557"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics revealed GOT1/ALDH3A1 pathway attenuated head and neck squamous cell carcinoma and increased cisplatin sensitivity through ROS induced by mitochondrial dysfunction.","authors":"Zhihui Liu, Baoai Han, Keshu Liu, Peng Zhou, Zehua Lin, Jiawen Li, Weisong Cai, Fangzi Ke, Yifan Hu, Jiahao Meng, Anbang Zhao, Shuang Li, Shuo Huang, Xiong Chen","doi":"10.1080/13510002.2025.2588031","DOIUrl":"10.1080/13510002.2025.2588031","url":null,"abstract":"<p><p>Current treatment options for head and neck squamous cell carcinoma (HNSCC) are limited. Aspartate aminotransaminase (GOT1) plays an important role in cancer development but its role in HNSCC remains unknown. We combined proteomics and metabolomics to identify high GOT1expression in human cancer tissues. The effects of GOT1 knockdown on cancer cell proliferation were confirmed using CCK8, wound healing assays, colony formation assays, and EdU assays. The anti-apoptotic ability of cancer cells was evaluated using TUNEL assay and flow cytometry. GOT1 knockdown caused mitochondrial dysfunction and was characterized by reduced mitochondrial membrane potential and altered expression of mitochondrial electron transport chain complexes and key transcription factors, as measured by JC-1 and qRT-PCR. Given that mitochondria are the primary source of reactive oxygen species (ROS), we assessed cellular ROS and mitochondrial superoxide levels by flow cytometry and found a significant increase. GOT1 knockdown increased the sensitivity of cells to cisplatin and decreased the volume of tumors in vivo. In summary, GOT1 knockdown inhibited proliferation and promoted apoptosis via ROS overproduction from mitochondrial dysfunction, thereby increasing cisplatin sensitivity. RNA-seq further identified aldehyde dehydrogenase 3A1 (ALDH3A1) as potentially downstream target of GOT1. These findings suggest that GOT1 knockdown may improve clinical outcomes in HNSCC.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2588031"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12671062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145655298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of oxidative stress and the Neuropilin-2-induced neuroinflammatory pathway by EMO ameliorates epileptic seizures in the preclinical model of epilepsy.","authors":"Haiting Li, Yujia Zhang, Yangyang Zhang, Yuehui Li, Huifang Wang","doi":"10.1080/13510002.2025.2547405","DOIUrl":"10.1080/13510002.2025.2547405","url":null,"abstract":"<p><strong>Objective: </strong>Epilepsy is a chronic neurological condition characterized by recurrent seizures, often linked to neuroinflammation and oxidative stress that exacerbate neuronal injury. Neuropilin-2 (NRP2) and Nuclear Factor-Kappa B (NF-κB) are key mediators in these pathways. This study evaluated the neuroprotective effects of emodin, a bioactive anthraquinone with antioxidant and anti-inflammatory properties, in a pentylenetetrazole (PTZ)-induced mouse model of epilepsy.</p><p><strong>Methods: </strong>Seizure severity, anxiety-like behavior (Elevated Plus Maze), and cognitive function (Morris Water Maze) were assessed. Oxidative stress markers including glutathione (GSH), catalase, lipid peroxidation (LPO), and glutathione-S-transferase (GST) were measured. Expression of NRP2, NF-κB, and proinflammatory cytokines (TNF-α, IL-6) was quantified. Docking studies examined emodin's binding affinity to NRP2 and NF-κB.</p><p><strong>Results: </strong>Emodin (200 mg/kg) significantly reduced seizure frequency and severity, improved anxiety-like behavior, and enhanced cognition. Biochemical analysis showed restored oxidative balance, with increased GSH and catalase activity and reduced LPO and GST dysfunction. Molecular studies revealed downregulation of NRP2, NF-κB, and cytokines. Docking confirmed strong binding affinity to NRP2 and NF-κB.</p><p><strong>Conclusion: </strong>Emodin alleviates oxidative stress and neuroinflammation by modulating NRP2 and NF-κB pathways, suggesting therapeutic potential in epilepsy.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2547405"},"PeriodicalIF":6.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12477776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}