Redox Report最新文献

Repurposing nitazoxanide as a novel ferroptosis inducer for triple-negative breast cancer via dual disruption of iron homeostasis and the β-catenin/GPX4 axis. 通过双重破坏铁稳态和β-catenin/GPX4轴，nitazoxanide作为一种新的三阴性乳腺癌铁凋亡诱导剂。

IF 6.9 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-06-29 DOI: 10.1080/13510002.2026.2695689

Chenshan Zhang, Ting Yang, Yuxuan Meng, Yao Zou, Ying Lu, Wenjun Wang, Sakorn Pornprasert, Wuga Jiwa, Tao He, Yan Lin

{"title":"Repurposing nitazoxanide as a novel ferroptosis inducer for triple-negative breast cancer via dual disruption of iron homeostasis and the β-catenin/GPX4 axis.","authors":"Chenshan Zhang, Ting Yang, Yuxuan Meng, Yao Zou, Ying Lu, Wenjun Wang, Sakorn Pornprasert, Wuga Jiwa, Tao He, Yan Lin","doi":"10.1080/13510002.2026.2695689","DOIUrl":"https://doi.org/10.1080/13510002.2026.2695689","url":null,"abstract":"Background: Ferroptosis induction is a promising triple-negative breast cancer (TNBC) therapy, but current inducers are suboptimal. Nitazoxanide (NTZ), an FDA-approved antiparasitic with anticancer and redox activity, may be repurposed as a ferroptosis inducer, yet its effects and mechanisms in TNBC are unclear.Methods: Anti-TNBC effects of NTZ were assessed in MDA-MB-231 and Hs578T cells via viability, clonogenicity, migration/invasion, and zebrafish xenografts. Ferroptosis was evaluated by iron levels, lipid peroxidation, GSH/GSSG, MDA, ROS, and mitochondrial TEM. Mechanisms were studied by docking, western blot, qPCR, apoptosis assay, cycloheximide chase, and pharmacological rescue.Results: NTZ inhibited proliferation, migration, and invasion in vitro and tumor growth in vivo, and induced ferroptosis. Mechanistically, it disrupted iron homeostasis by upregulating TFR1 and downregulating FPN1, causing iron overload and lipid peroxidation, and promoted β-catenin degradation, which transcriptionally suppressed GPX4, weakening antioxidant defense. Both β-catenin stabilization and ferroptosis inhibition reversed these effects.Conclusion: NTZ is repurposed as a ferroptosis inducer for TNBC via dual disruption of iron homeostasis and β-catenin/GPX4 axis, providing a strong preclinical rationale for its therapeutic use.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2695689"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148346206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction. 修正。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-03-12 DOI: 10.1080/13510002.2026.2645268

引用次数: 0

Correction. 修正。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-03-24 DOI: 10.1080/13510002.2026.2648349

引用次数: 0

Bilirubin reduces mortality in sepsis models by inhibiting NOX2-mediated formation of neutrophil extracellular traps. 胆红素通过抑制nox2介导的中性粒细胞胞外陷阱的形成，降低败血症模型的死亡率。

IF 6.9 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-04-28 DOI: 10.1080/13510002.2026.2664962

Sang-Jin Kim, Chang Woo Ko, Wan-Seo Kim, Yeon Jun Kang, Chul-Hwan Lee, Won-Woo Lee, Jong-Wan Park

{"title":"Bilirubin reduces mortality in sepsis models by inhibiting NOX2-mediated formation of neutrophil extracellular traps.","authors":"Sang-Jin Kim, Chang Woo Ko, Wan-Seo Kim, Yeon Jun Kang, Chul-Hwan Lee, Won-Woo Lee, Jong-Wan Park","doi":"10.1080/13510002.2026.2664962","DOIUrl":"10.1080/13510002.2026.2664962","url":null,"abstract":"Objectives: Sepsis is a life-threatening condition driven by a dysregulated immune response to infection, yet therapeutic options beyond antibiotics and vasopressors remain limited. Neutrophil extracellular traps (NETs) contribute significantly to sepsis-induced tissue injury, and NETosis inhibition has emerged as a potential therapeutic strategy. We hypothesized that the endogenous metabolite bilirubin mitigates inflammation in sepsis by inhibiting NETosis through targeting NOX2.Methods: Two murine sepsis models were used to assess the effects of bilirubin on survival and systemic NETosis. Plasma NET biomarkers were quantified, and primary human neutrophils were used to validate the NETosis-inhibitory activity of bilirubin in vitro. Mechanistic studies included ROS measurements, NOX2 loop C mutational analysis, and inhibition of endocytosis and autophagy to examine how bilirubin modulates NOX2 stability.Results: Bilirubin improved survival and reduced NET biomarkers in both models. It inhibited NETosis in human neutrophils by suppressing ROS-dependent NETosis and promoting the internalization and degradation of NOX2 via endocytosis and autophagy.Discussion: These findings identify bilirubin as an endogenous inhibitor of NETosis. By targeting NOX2 and suppressing NETosis, bilirubin may represent a promising therapeutic candidate for sepsis management.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2664962"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779252","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}

引用次数: 0

Sirtuin 5-mediated desuccinylation of PRDX6 inhibits ferroptosis and alleviates sepsis-associated acute kidney injury. Sirtuin 5介导的PRDX6去琥珀酰化抑制铁下垂并减轻脓毒症相关急性肾损伤。

IF 6.9 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-04-10 DOI: 10.1080/13510002.2026.2657075

Wenlong Lin, Caitao Dong, Qinhong Jiang, Yuanquan Lou, Long Wang, Ziqi He

{"title":"Sirtuin 5-mediated desuccinylation of PRDX6 inhibits ferroptosis and alleviates sepsis-associated acute kidney injury.","authors":"Wenlong Lin, Caitao Dong, Qinhong Jiang, Yuanquan Lou, Long Wang, Ziqi He","doi":"10.1080/13510002.2026.2657075","DOIUrl":"10.1080/13510002.2026.2657075","url":null,"abstract":"Objectives: To investigate the role of the SIRT5-PRDX6 axis during the pathogenesis of sepsis-associated acute kidney injury (SA-AKI).Methods: In vivo and in vitro sepsis models were established to evaluate oxidative stress and inflammatory responses. High-throughput proteomics analysis identified ferroptosis as a key mechanism underlying SA-AKI. The levels of HMOX1, NQO-1, GPX4, ACSL4, Fe²⁺, IL-1β, TNF-α, MDA, and GSH were measured. SIRT5 knockdown/overexpression experiments were performed in HK-2 cells, and SIRT5-deficient mice were used to explore its regulatory role. Co-immunoprecipitation (Co-IP) and site-directed mutagenesis verified SIRT5-PRDX6 interaction and desuccinylation sites.Results: Ferroptosis was critical in SA-AKI progression. In LPS-induced HK-2 cells, HMOX1, NQO-1, ACSL4, Fe²⁺, IL-1β, TNF-α, and MDA were significantly increased, whereas GSH and GPX4 were downregulated. Treatment with ferrostatin-1 (Fer-1) attenuated ferroptosis and oxidative damage. SIRT5 decreased in a time-dependent manner following LPS stimulation. SIRT5 knockdown exacerbated LPS-induced ferroptosis, whereas SIRT5 overexpression suppressed it. SIRT5 activation alleviated AKI in mice, whereas SIRT5 deficiency aggravated it. Mechanistically, SIRT5 desuccinylated PRDX6 at lysine 209, thereby inhibiting inflammatory and oxidative stress responses, attenuating ferroptosis, and ultimately ameliorating renal injury.Conclusion: The SIRT5-PRDX6 axis regulates SA-AKI pathogenesis by modulating ferroptosis and represents a novel potential therapeutic target.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2657075"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13072693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645459","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}

引用次数: 0

Type III intermediate filaments as novel CoAlation targets. III型中间细丝作为新的coalition靶点。

IF 6.9 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-06-24 DOI: 10.1080/13510002.2026.2692797

Nuria Goya-Iglesias, Bess Yi Kun Yu, Ivan Gout, Dolores Pérez-Sala

{"title":"Type III intermediate filaments as novel CoAlation targets.","authors":"Nuria Goya-Iglesias, Bess Yi Kun Yu, Ivan Gout, Dolores Pérez-Sala","doi":"10.1080/13510002.2026.2692797","DOIUrl":"10.1080/13510002.2026.2692797","url":null,"abstract":"Objectives: Type III intermediate filaments, such as vimentin, GFAP, and desmin, are involved in cell mechanics, signaling, and stress responses, and are tightly regulated by posttranslational modifications (PTMs). The monomers of these proteins possess a single cysteine residue that plays a key role in network remodeling under oxidative stress. CoAlation is a PTM involving mixed disulfide bond formation between a protein thiol and the coenzyme A (CoA) thiol. Here we aim to investigate the potential CoAlation of vimentin, GFAP, and desmin, and its functional consequences.Methods: CoAlation of type III intermediate filaments and its interplay with other oxidative modifications was assessed in vitro by gel assays and immunological detection, whereas its effect on vimentin filament assembly was evaluated by electron microscopy. In cells, CoAlation was evaluated by CoA immunofluorescence, proximity ligation assay, and/or immunoprecipitation.Results: CoAlation of vimentin, GFAP, and desmin occurs in vitro and in cells, and is enhanced by oxidants. In the case of vimentin, CoA reciprocally influences other thiol group modifications in vitro, attenuating disulfide-mediated oligomerization and cysteine alkylation. Moreover, in vitro polymerization in the presence of CoA results in shorter vimentin filaments.Conclusion: We show that vimentin, GFAP, and desmin are CoAlated at their single cysteine residues. Our results suggest that CoAlation may influence filament assembly and compete with other cysteine modifications. Moreover, given its reversibility, CoAlation could potentially play a protective role against more deleterious modifications, such as irreversible cysteine oxidation.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2692797"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13307387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318856","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}

引用次数: 0

Cr(VI) and DON co-exposure triggers intestinal epithelial cells ferroptosis and pyroptosis through Nrf2/NF-κB/NLRP3 to impair intestinal barrier function. Cr（VI）和DON共暴露可通过Nrf2/NF-κB/NLRP3触发肠上皮细胞铁亡和焦亡，损害肠屏障功能。

IF 6.9 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-09-03 DOI: 10.1080/13510002.2026.2724639

Yueming Gu, Xinyuan Miao, Linrui Fan, Guodong Cai, Ruilong Song, Hui Zou, Jianhong Gu, Yan Yuan, Xuezhong Liu, Zongping Liu, Jianchun Bian

{"title":"Cr(VI) and DON co-exposure triggers intestinal epithelial cells ferroptosis and pyroptosis through Nrf2/NF-κB/NLRP3 to impair intestinal barrier function.","authors":"Yueming Gu, Xinyuan Miao, Linrui Fan, Guodong Cai, Ruilong Song, Hui Zou, Jianhong Gu, Yan Yuan, Xuezhong Liu, Zongping Liu, Jianchun Bian","doi":"10.1080/13510002.2026.2724639","DOIUrl":"10.1080/13510002.2026.2724639","url":null,"abstract":"Objectives: Cr(VI) and DON are natural co-occurring pollutants in the environment. This study aimed to investigate the molecular mechanisms underlying oxidative damage to the intestinal barrier and intestinal epithelial cell (IECs) toxicity induced by Cr(VI) and DON.Methods: The target genes and signaling pathways were predicted using the network toxicology method. This was verified through cell intervention experiments with Nrf2 activator TBHQ, NF-κB inhibitor PDTC, and NLRP3 inhibitor MCC950.Results: Cr(VI) and/or DON aggravated inflammatory infiltration in the intestine, disrupted tight junction structures. Network toxicology revealed that ferroptosis and pyroptosis pathways are involved in regulating oxidative damage and barrier dysfunction in primary small IECs in broilers. Cr(VI) and/or DON induced oxidative stress and inhibited Nrf2 expression. They abnormally activated the NF-κB/NLRP3 pathway in IECs, thereby triggering ferroptosis and pyroptosis, and exacerbating oxidative damage to the intestinal barrier. Overexpression of Nrf2 and silencing of NLRP3/NF-κB could bidirectionally reverse oxidative stress, iron accumulation, inflammatory factor secretion and intestinal barrier dysfunction in IECs, inhibit the progression of ferroptosis and pyroptosis.Conclusion: The cross-regulation of ferroptosis and pyroptosis mediated by the bidirectional imbalance of the Nrf2/NF‑κB/NLRP3 axis constitutes the core molecular mechanism underlying intestinal epithelial barrier dysfunction and oxidative damage induced by co-exposure to Cr(VI) and DON.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2724639"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13543835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888481","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}

引用次数: 0

EGCG-loaded nanoparticles attenuate post-SAH white matter injury by targeting HO-1/S100A10 to suppress oxidative stress-induced reactive astrocytes. 负载egcg的纳米颗粒通过靶向HO-1/S100A10抑制氧化应激诱导的反应性星形胶质细胞，减轻sah后白质损伤。

IF 6.9 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-04-28 DOI: 10.1080/13510002.2026.2664955

Dongcen Lang, Yanning Zheng, Jing Zhang, Zheng Li, Mengyu Niu, Jian Wang, Xue Wang, Liyong Huang, Jiangyu Xue, Li Li, Ying Chen

{"title":"EGCG-loaded nanoparticles attenuate post-SAH white matter injury by targeting HO-1/S100A10 to suppress oxidative stress-induced reactive astrocytes.","authors":"Dongcen Lang, Yanning Zheng, Jing Zhang, Zheng Li, Mengyu Niu, Jian Wang, Xue Wang, Liyong Huang, Jiangyu Xue, Li Li, Ying Chen","doi":"10.1080/13510002.2026.2664955","DOIUrl":"10.1080/13510002.2026.2664955","url":null,"abstract":"Objective: Subarachnoid hemorrhage (SAH) is associated with high mortality and poor outcomes, which are closely related to white matter injury (WMI). (-)-Epigallocatechin-3-gallate (EGCG) exerts neuroprotective effects by inhibiting oxidative stress-related ferroptosis in astrocytes and improving neurological function. However, the role and mechanism of EGCG in regulating reactive astrocytes (RAs) to alleviate WMI after SAH remain unclear.Methods: A mouse model of SAH was used to evaluate the effects of EGCG-loaded nanoparticles (EGCG-NPs). Western blot, qPCR, and immunofluorescence were performed for biochemical analysis. Neurological function was assessed using neurological deficit scores and the Morris water maze test.Results: Following SAH, HO-1-mediated iron accumulation and ROS production promoted A1/A2 reactive astrocyte polarization, resulting in myelination damage and aggravated WMI. Knockdown of S100A10 inhibited iron-dependent oxidative stress in RAs and attenuated WMI. EGCG-NPs significantly suppressed HO-1/S100A10-mediated iron overload and oxidative stress in both A1 and A2 RAs, thereby alleviating WMI after SAH.Conclusion: EGCG-NPs attenuate SAH-induced WMI by inhibiting the iron overload-activated HO-1/S100A10 axis in RAs, representing a promising therapeutic strategy.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2664955"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779390","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}

引用次数: 0

Coordinated mitochondrial quality control underlies oxidative stress resilience in MUSE stem cells. 协调线粒体质量控制是缪斯干细胞氧化应激恢复能力的基础。

IF 6.9 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-10-09 DOI: 10.1080/13510002.2026.2698189

Domenico Aprile, Sura Hilal Ahmed Al-Sammarraie, Alessia Ambrosino, Mohd Shahzaib, Yesuf Siraj, Afshin Samiminemati, Nicola Alessio, Gianfranco Peluso, Giovanni Di Bernardo, Umberto Galderisi

{"title":"Coordinated mitochondrial quality control underlies oxidative stress resilience in MUSE stem cells.","authors":"Domenico Aprile, Sura Hilal Ahmed Al-Sammarraie, Alessia Ambrosino, Mohd Shahzaib, Yesuf Siraj, Afshin Samiminemati, Nicola Alessio, Gianfranco Peluso, Giovanni Di Bernardo, Umberto Galderisi","doi":"10.1080/13510002.2026.2698189","DOIUrl":"10.1080/13510002.2026.2698189","url":null,"abstract":"Background: Reactive oxygen species (ROS) regulate stem-cell function, but sustained exposure causes oxidative damage, mitochondrial dysfunction and exhaustion. Multilineage-differentiating Stress-Enduring (MUSE) cells, a rare SSEA-3⁺ MSC subset, tolerate ROS-rich environments, although the mechanisms remain unclear.Methods: We compared MUSE, Non-MUSE (SSEA-3⁻) and MSCs after H₂O₂ exposure, assessing ROS clearance, mtDNA integrity, 8-oxo-dG, antioxidant and BER responses, mitochondrial morphology/function, mitophagy and biogenesis, with focus on the PGC-1α/NRF2 axis. Three independent biological replicates were analyzed by imaging, qPCR, flow cytometry and biochemical assays.Results: MUSE cells showed greater resistance to oxidative stress than MSCs and Non-MUSE cells. After H₂O₂, they displayed lower ROS accumulation (~15-25%), preserved mtDNA integrity, reduced 8-oxo-dG, rapid induction of antioxidant and BER-related genes, and maintenance of mitochondrial morphology, membrane potential and respiratory activity. MUSE cells also showed enhanced mitophagy, with >2-fold increased LAMP1-MitoTracker colocalization and induction of PINK1/phospho-Ub-S65, together with increased biogenesis, including ~45% higher COX-I/SDHA ratio, TFAM induction and PGC-1α activation at 48 h.Conclusion: MUSE cells coordinate antioxidant defense, DNA repair, mitophagy and biogenesis through a remove-and-replace program that preserves mitochondrial function during oxidative stress.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2698189"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13656651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149138146","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}

引用次数: 0

Protective effects of Angelica dahurica polysaccharide on oxidative stress and liver injury induced by ovariectomized/D-galactose in rats. 白芷多糖对去卵巢/ d -半乳糖所致大鼠氧化应激及肝损伤的保护作用。

IF 6.9 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-05-20 DOI: 10.1080/13510002.2026.2674473

Xue-Qin He, Yi-Zhang Li, Li-Ba Xu, Chun-Feng Wu, Du-Dong Wei, Hao-Yu Liu, Fen Qiu

{"title":"Protective effects of Angelica dahurica polysaccharide on oxidative stress and liver injury induced by ovariectomized/D-galactose in rats.","authors":"Xue-Qin He, Yi-Zhang Li, Li-Ba Xu, Chun-Feng Wu, Du-Dong Wei, Hao-Yu Liu, Fen Qiu","doi":"10.1080/13510002.2026.2674473","DOIUrl":"10.1080/13510002.2026.2674473","url":null,"abstract":"Background: Oxidative stress-induced liver injury can progress to severe hepatic conditions. Polysaccharides are promising therapeutic agents, but the protective effects of Angelica dahurica polysaccharide (ADP) against this injury remain unclear.Purpose: This study was conducted to elucidate ADP's protective effects and underlying molecular mechanisms in Ovariectomize/D-galactose (OVX/D-Gal) rats.Methods: Fifty female OVX rats and ten sham-operated (SO) rats were randomly divided into six groups. Except SO group, rats were administered the corresponding doses of ADP and resveratrol respectively, and the model was established by 49-day daily subcutaneous D-Gal injection. Serum and liver samples were collected to examine the hepatic histopathological changes, oxidative stress-related biomarkers, inflammatory factors, and protein and gene expression levels.Results: ADP reduced serum ALT and AST levels (P < 0.01) and improved liver histology. ADP increased SOD and GSH-Px activities , decreased MDA levels (P < 0.05). ADP also lowered pro-inflammatory cytokines levels, upregulated Nrf2, HO-1, and NQO-1 expression, promoted Bcl-2 and suppressed Bax and cleaved caspase-3 (P < 0.05).Conclusions: ADP alleviated OVX/D-Gal-induced oxidative stress and liver injury by increasing antioxidant capacity, inhibiting apoptosis, attenuating inflammation, and activating Nrf2/HO-1/NQO-1 signaling pathway.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2674473"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13192090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974967","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}

引用次数: 0