Redox Report最新文献_第10页

Recent advances in the investigation of the regulatory network underlying reactive nitrogen species-mediated tumorigenesis: molecular mechanisms and targeted therapeutic strategies. 活性氮物种介导肿瘤发生的调控网络研究进展：分子机制和靶向治疗策略。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-10-02 DOI: 10.1080/13510002.2025.2564593

Yimao Wu, Zichang Chen, Xiaoyan Chen, Yinting Hu, Yunqi Ma

{"title":"Recent advances in the investigation of the regulatory network underlying reactive nitrogen species-mediated tumorigenesis: molecular mechanisms and targeted therapeutic strategies.","authors":"Yimao Wu, Zichang Chen, Xiaoyan Chen, Yinting Hu, Yunqi Ma","doi":"10.1080/13510002.2025.2564593","DOIUrl":"10.1080/13510002.2025.2564593","url":null,"abstract":"Reactive nitrogen species (RNS) play a pivotal role in tumorigenesis through complex regulatory networks within the tumor microenvironment (TME). This review summarizes recent advances in understanding RNS-mediated mechanisms, focusing on core components and their concentration-dependent bidirectional effects on tumor cell proliferation, apoptosis, invasion, and metabolism. It explores RNS sources in the TME, including autonomous synthesis by tumor cells and secretion by immune cells (e.g., TAMs, TANs), and their modulation of key signaling pathways (e.g., PI3 K/Akt, NF-κB, HIF-1α). Additionally, the review discusses RNS-mediated regulation of immune responses and angiogenesis, highlighting their dual roles in promoting tumor progression and enabling immune evasion. Finally, it outlines potential clinical applications, such as RNS-targeted diagnostic probes and therapeutic strategies (e.g., iNOS inhibitors, NO donors), providing a foundation for precision oncology.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2564593"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12493636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207366","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

Verbascoside targets endothelial HIF-1α/ Lysyl oxidase signaling to attenuate glomerular injury in diabetic nephropathy. 毛蕊花苷靶向内皮HIF-1α/赖氨酸氧化酶信号减轻糖尿病肾病肾小球损伤

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-12-08 DOI: 10.1080/13510002.2025.2598110

Tianyu Kang, Bin Hou, Min Shi, Huan Liu, Yanan Li, Kaixin Li, Shuxin Li, Zetong Wu, Zhaopeng Xu, Mengnan Li

{"title":"Verbascoside targets endothelial HIF-1α/ Lysyl oxidase signaling to attenuate glomerular injury in diabetic nephropathy.","authors":"Tianyu Kang, Bin Hou, Min Shi, Huan Liu, Yanan Li, Kaixin Li, Shuxin Li, Zetong Wu, Zhaopeng Xu, Mengnan Li","doi":"10.1080/13510002.2025.2598110","DOIUrl":"10.1080/13510002.2025.2598110","url":null,"abstract":"Background: Diabetic nephropathy (DN) drives progressive renal fibrosis and functional decline, ultimately leading to end-stage renal disease. Pathological crosstalk between glomerular endothelial cells and mesangial cells is increasingly recognized as central to DN progression. However, whether endothelial-derived signaling specifically drives mesangial injury under diabetic conditions remains undefined.Methods: We applied multi-omics profiling to identify pathogenic drivers. Target validation included qPCR and immunofluorescence co-localization in renal tissues. In vitro endothelial-mesangial crosstalk was modeled using conditioned media (CM) from mouse GECs applied to mesangial cells. Verbascoside (VB) was screened via structure-based virtual docking against LOX/LOXL2 and binding affinity (KD) confirmed by biolayer interferometry (BLI). In vivo therapeutic efficacy of VB was assessed in db/db mice.Results: LOX/LOXL2 was robustly upregulated in diabetic endothelia. Inhibiting endothelial-derived LOX/LOXL2 or HIF-1α in GECs attenuated HG-induced mesangial dysfunction by reducing proliferation/viability, oxidative stress, and fibrosis. Mechanistically, HIF-1α drove LOX/LOXL2 expression. VB was identified as a novel dual LOX/LOXL2 inhibitor. VB-CM mitigated mesangial injury in vitro. VB treatment improved renal function, reduced oxidative damage, and ameliorated fibrosis.Conclusion: Endothelial HIF-1α/LOX signaling drives mesangial oxidative stress and fibrosis in DN. Verbascoside, a dual LOX/LOXL2 inhibitor, represents a promising therapeutic agent targeting this pathogenic axis.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2598110"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12687904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145701553","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

Ginkgo biloba attenuates complete Freund's adjuvant-induced inflammatory pain by suppressing the NF-κB-CXCL1/CXCR2 signaling cascade in the rat spinal cord. 银杏叶通过抑制大鼠脊髓NF-κB-CXCL1/CXCR2信号级联减轻完全Freund佐剂诱导的炎症性疼痛。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2024-12-31 DOI: 10.1080/13510002.2024.2447778

Sherine Abdel Salam, Catherine S George, Najla K Al Abdulsalam, Ashraf M Abdel-Moneim, Amina E Essawy

{"title":"Ginkgo biloba attenuates complete Freund's adjuvant-induced inflammatory pain by suppressing the NF-κB-CXCL1/CXCR2 signaling cascade in the rat spinal cord.","authors":"Sherine Abdel Salam, Catherine S George, Najla K Al Abdulsalam, Ashraf M Abdel-Moneim, Amina E Essawy","doi":"10.1080/13510002.2024.2447778","DOIUrl":"10.1080/13510002.2024.2447778","url":null,"abstract":"Background: Inflammatory pain is the most common type of chronic pain, and it is rapidly becoming a global health problem. Ginkgo biloba (EGb761) is a natural plant that contains several bioactive components with antioxidant and free radical scavenging properties. However, its underlying mechanism in inflammatory pain remains unclear. The aim of this study was to assess the effects and mechanisms of EGb761 on a complete Freund's adjuvant (CFA)-induced inflammatory pain model in rats.Methods: A single dose of CFA was subcutaneously injected into the right hind paws of the rats, after which EGb761 (100 mg/kg/day) was orally administered for 14 days.Results: Oral EGb761 markedly decreased hind paw edema in CFA-treated rats. In addition, EGb761 significantly reduced thermal hyperalgesia by increasing the hot plate latency and improved motor coordination. Notably, EGb761 significantly reduced nitric oxide levels and catalase enzyme activity in the lumbar spinal cord (LSPC) of CFA-treated rats. Furthermore, EGb761 inhibited the mRNA expression of NF-ĸB, CXCL1, and CXCR2. At the histological level, EGb761 prevented CFA-induced tissue and neuronal damage in the LSPC dorsal horn. The immunohistochemical analysis revealed that caspase-3 levels were significantly reduced, whereas Bcl-2 expression was insignificantly increased with EGb761 treatment in rats with CFA-induced inflammation.Conclusion: EGb761 alleviated CFA-induced chronic inflammatory pain by attenuating oxidant-antioxidant dysregulation, blocking the NF-κB-CXCL1/CXCR2 inflammatory axis, and counteracting neural cell apoptosis in the LSPC. Our results suggest that EGb761 can be used as an analgesic for the treatment of pain associated with inflammation and tissue injury.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2447778"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11703301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145701595","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

Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway. 高同型半胱氨酸血症通过抑制Nrf2/HO-1信号通路加重牙周炎。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-03-09 DOI: 10.1080/13510002.2025.2475691

Kaiqiang Yang, Yuting Yang, Ting Long, Xiaoxue Wang, Yeke Chen, Chenjiang He, Li Li, Xinbo Yang, Meixiu Jiang, Yichen Hu, Fang Dai, Li Song

{"title":"Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway.","authors":"Kaiqiang Yang, Yuting Yang, Ting Long, Xiaoxue Wang, Yeke Chen, Chenjiang He, Li Li, Xinbo Yang, Meixiu Jiang, Yichen Hu, Fang Dai, Li Song","doi":"10.1080/13510002.2025.2475691","DOIUrl":"10.1080/13510002.2025.2475691","url":null,"abstract":"Periodontitis, a common dental illness, causes periodontal tissue inflammation and irreversible bone loss, inevitably resulting in tooth loss. Hyperhomocysteinaemia (HHcy), defined as blood total homocysteine (Hcy) levels greater than 15 µmol/L, is linked to increased cardiovascular disease risk. Mounting evidence indicates a connection between HHcy and periodontitis; however, the underlying processes remain unknown. Herein, we explored the mechanisms by which HHcy exacerbates periodontal tissue inflammation and osteoclast formation. In an animal model of periodontitis treated with HHcy, periodontal attachment loss was aggravated, and both systemic and gingival tissue inflammation levels tended to increase; additionally, antioxidant-related proteins were suppressed and expressed at low levels, whereas oxidative damage-related protein expression increased. In RAW264.7 cells treated with LPS or LPS + Hcy, the LPS + Hcy group presented increased reactive oxygen species (ROS) fluorescence intensity, and Nrf2/HO-1 signalling pathway suppression was associated with inflammatory cytokine (TNF-α) expression. In monocyte osteoclasts treated with Rankl or Rankl + Hcy, the Rankl + Hcy group presented Nrf2/HO-1 signalling pathway suppression, an increase in osteoclast-related proteins (NFATc-1 and CTSK), and a more pronounced osteoclastic phenotype. Therefore, HHcy may exacerbate inflammation severity and osteoclast generation in periodontitis by promoting ROS production and inhibiting the Nrf2/HO-1 signalling pathway.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2475691"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586768","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

Dynamic redox monitoring in differentiated human neuroblastoma models of Parkinson's disease. 帕金森病分化人神经母细胞瘤模型的动态氧化还原监测。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 DOI: 10.1080/13510002.2025.2595781

Jungeun Lim, Xavier Zhou, Srija Pamujula, Rukkia Liaqat, Ananya Achanta, Loren Looger, Benjamin C Campbell, Melissa M Campbell

{"title":"Dynamic redox monitoring in differentiated human neuroblastoma models of Parkinson's disease.","authors":"Jungeun Lim, Xavier Zhou, Srija Pamujula, Rukkia Liaqat, Ananya Achanta, Loren Looger, Benjamin C Campbell, Melissa M Campbell","doi":"10.1080/13510002.2025.2595781","DOIUrl":"10.1080/13510002.2025.2595781","url":null,"abstract":"Background: Oxidative stress plays a critical role in the degeneration of midbrain dopaminergic (DA) neurons in Parkinson's disease (PD). However, therapies targeting redox mechanisms are hindered by a lack of scalable and inexpensive redox-focused preclinical models.Methods: We stably expressed the glutathione-specific redox-sensitive fluorescent protein Grx-roGFP2 in SH-SY5Y and BE(2)-M17 neuroblastoma cell lines. We developed an improved differentiation protocol using staurosporine and dbcAMP to enhance dopaminergic-like characteristics, assessed by DA marker expression, and characterized responses to PD-relevant toxins.Results: BE(2)-M17 cells expressed higher DA markers than SH-SY5Y cells, and the improved protocol further increased DA markers. Differentiated neuroblastoma cells with dopaminergic-like features showed greater sensitivity to MPP+ and paraquat, with reduced viability, increased oxidative stress, glutathione oxidation, decreased TH expression, and altered neuronal morphology, paralleling patterns observed in PD-related oxidative injury. roGFP2 enabled robust, real-time redox monitoring, correlating oxidative stress with phenotype. Sublethal toxin exposure caused mitochondrial alterations and redox shifts. Pretreatment with N-acetyl-L-cysteine (NAC) mitigated oxidative stress, improved viability, and partially restored TH expression and morphology.Conclusion: This neuroblastoma-based model with dopaminergic-like features enables scalable, real-time redox monitoring and detailed phenotypic analyses. It expands access to redox biology platforms for investigating neurodegeneration and evaluating antioxidant therapeutic strategies relevant to neurodegeneration.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2595781"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12671422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145655286","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

The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells. PKC/NOX/ROS和PYK2/MEK/ERK/PARP信号通路驱动小胶质细胞非细胞溶解性氧化应激诱导的TRPM2通道激活。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-05-15 DOI: 10.1080/13510002.2025.2503131

Sharifah Alawieyah Syed Mortadza, Nur Zulaikha Mohamad Zahir, Chew Tze Wei, Lin-Hua Jiang

{"title":"The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells.","authors":"Sharifah Alawieyah Syed Mortadza, Nur Zulaikha Mohamad Zahir, Chew Tze Wei, Lin-Hua Jiang","doi":"10.1080/13510002.2025.2503131","DOIUrl":"10.1080/13510002.2025.2503131","url":null,"abstract":"Objectives: The study aimed to investigate the signalling mechanism for TRPM2 channel activation by non-cytolytic oxidative stress in microglia.Methods: Microglia from wild-type (WT) and TRPM2-knockout (KO) mice were exposed to 10-30 mM H2O2 for up to 24 hours. Morphological changes characteristic of microglial activation, [Ca2+]c, ROS generation and the effects of inhibiting particular signalling pathways were examined.Results: Exposure of WT microglia to H2O2 for 24 hours caused no cell death but induced salient morphological changes, which was prevented by TRPM2-KO. Exposure of WT microglia to H2O2 to 2 hours failed, and extension to 8 hours was required, to induce an increase in [Ca2+]c, which was abolished by TRPM2-KO. Exposure of microglia to H2O2 for 8 hours induced ROS generation, which was suppressed by inhibition of PKC and NADPH oxidases (NOX). H2O2-induced PARP activation in TRPM2-KO cells was lower than that in WT cells. Furthermore, H2O2-induced activation of PARP and TRPM2 and morphological changes were attenuated by inhibition of PCK and NOX as well as PYK2 and MEK/ERK.Conclusion: Our results support that PKC/NOX-mediated ROS generation and TRPM2-mediated Ca2+-induced activation of the PYK2/MEK/ERK pathway form a positive feedback mechanism to drive TRPM2 channel activation by non-cytolytic oxidative stress.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2503131"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12086945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079879","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

Therapeutic combination of L-ascorbic acid, N-acetylcysteine, and dimethyl fumarate in Friedreich's ataxia: insights from in vitro models. l -抗坏血酸、n -乙酰半胱氨酸和富马酸二甲酯联合治疗弗里德赖希共济失调：来自体外模型的见解。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-05-15 DOI: 10.1080/13510002.2025.2505303

Fred Jonathan Edzeamey, Zenouska Ramchunder, Adamo Valle Gómez, Haobo Ge, Carlo Marya Thomas Marobbio, Charareh Pourzand, Sara Anjomani Virmouni

{"title":"Therapeutic combination of L-ascorbic acid, N-acetylcysteine, and dimethyl fumarate in Friedreich's ataxia: insights from in vitro models.","authors":"Fred Jonathan Edzeamey, Zenouska Ramchunder, Adamo Valle Gómez, Haobo Ge, Carlo Marya Thomas Marobbio, Charareh Pourzand, Sara Anjomani Virmouni","doi":"10.1080/13510002.2025.2505303","DOIUrl":"10.1080/13510002.2025.2505303","url":null,"abstract":"Friedreich's Ataxia (FRDA) is a rare neurological disorder caused by an abnormal expansion of Guanine-Adenine-Adenine (GAA) repeat in intron 1 of the FXN gene, which encodes frataxin, leading to reduced expression of frataxin, a mitochondrial protein essential for cellular homeostasis. Frataxin deficiency results in oxidative stress and mitochondrial dysfunction and impaired redox balance. Currently, there is no cure for FRDA. This study aimed to evaluate the therapeutic potential of antioxidants dimethyl fumarate (DMF), N-acetylcysteine (NAC), and L-ascorbic acid (LAA) in restoring mitochondrial redox homeostasis and frataxin levels in FRDA patient-derived fibroblasts and 2D sensory neurons. We assessed cell viability, mitochondrial and cellular reactive oxygen species (ROS) levels, mitochondrial DNA copy number, mitochondrial membrane potential, and frataxin and NRF2 expression at both mRNA and protein levels following antioxidant treatment, either individually or in combination. Treatment with LAA, NAC, and DMF resulted in significant reductions in mitochondrial and cellular ROS, along with increased FXN and NRF2 expression, and enhanced NRF2 nuclear translocation. Furthermore, these compounds improved aconitase/citrate synthase activity, GSH/GSSG ratios, and mitochondrial membrane potential. Notably, the combination of LAA and NAC consistently alleviated multiple disease-associated defects in FRDA cells, suggesting its potential as a promising therapeutic approach.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2505303"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12082744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079882","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

Flavonoids from Polypodium hastatum as neuroprotective agents attenuate cerebral ischemia/reperfusion injury in vitro and in vivo via activating Nrf2. 黄酮类化合物在体外和体内通过激活Nrf2减轻脑缺血再灌注损伤的作用。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2024-12-19 DOI: 10.1080/13510002.2024.2440204

Huankai Yao, Ruiqing Wu, Dan Du, Fengwei Ai, Feng Yang, Yan Li, Suhua Qi

{"title":"Flavonoids from Polypodium hastatum as neuroprotective agents attenuate cerebral ischemia/reperfusion injury in vitro and in vivo via activating Nrf2.","authors":"Huankai Yao, Ruiqing Wu, Dan Du, Fengwei Ai, Feng Yang, Yan Li, Suhua Qi","doi":"10.1080/13510002.2024.2440204","DOIUrl":"https://doi.org/10.1080/13510002.2024.2440204","url":null,"abstract":"Objectives: Cerebral ischemic stroke is a leading cause of death worldwide. Though timely reperfusion reduces the infarction size, it exacerbates neuronal apoptosis due to oxidative stress. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor regulating the expression of antioxidant enzymes. Activating Nrf2 gives a therapeutic approach to ischemic stroke.Methods: Herein we explored flavonoids identified from Polypodium hastatum as Nrf2 activators and their protective effects on PC12 cells injured by oxygen and glucose deprivation/restoration (OGD/R) as well as middle cerebral artery occlusion (MCAO) mice.Results: The results showed among these flavonoids, AAKR significantly improved the survival of PC12 cells induced by OGD/R and activated Nrf2 in a Keap1-dependent manner. Further investigations have disclosed AAKR attenuated oxidative stress, mitochondrial dysfunction and following apoptosis resulting from OGD/R. Meanwhile, activation of Nrf2 by AAKR was involved in the protective effects. Finally, it was found that AAKR could protect MCAO mice brains against ischemia/reperfusion injury via activating Nrf2.Discussion: This investigation could provide lead compounds for the discovery of novel Nrf2 activators targeting ischemia/reperfusion injury.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2440204"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865467","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

Norepinephrine promotes oxidative stress in vascular adventitial fibroblasts via PKC/NFκB-mediated NOX2 upregulation. 去甲肾上腺素通过PKC/ nfκ b介导的NOX2上调促进血管外成纤维细胞的氧化应激。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-23 DOI: 10.1080/13510002.2025.2494314

Yi-Ming Wang, Hong-Ke Dong, Min Dai, Jing-Xiao Wang, Xiao-Yu Xu, Guo-Qing Zhu, Xiu-Zhen Li

{"title":"Norepinephrine promotes oxidative stress in vascular adventitial fibroblasts via PKC/NFκB-mediated NOX2 upregulation.","authors":"Yi-Ming Wang, Hong-Ke Dong, Min Dai, Jing-Xiao Wang, Xiao-Yu Xu, Guo-Qing Zhu, Xiu-Zhen Li","doi":"10.1080/13510002.2025.2494314","DOIUrl":"https://doi.org/10.1080/13510002.2025.2494314","url":null,"abstract":"Background: Sympathetic overactivity is closely associated with vascular remodeling. Sympathetic fibers dominantly innervate the adventitia of arteries rather than tunica media. Vascular adventitial fibroblasts (VAFs) play crucial roles in vascular remodeling. However, the link between sympathetic overactivity and VAF proliferation and migration is unknown.Methods: Primary VAFs were isolated from the thoracic aorta of spontaneously hypertensive rats and Wistar-Kyoto rats. Norepinephrine (NE) bitartrate monohydrate was applied to VAFs to simulate the sympathetic overactivity.Results: NE increased NADPH oxidase (NOX) 2 expression and superoxide level, which were almost abolished by NOX2 inhibitor GSK2795039 or α-adrenoceptor antagonist prazosin, but not significantly affected by NOX1 inhibitor ML171, NOX4 inhibitor GLX351322 or β-adrenoceptor antagonist propranolol. Superoxide scavenger tempol or NOX2 inhibitor GSK2795039 attenuated NE-induced VAF proliferation and migration. NE promoted protein kinase C (PKC) phosphorylation and NFκB-p65 nuclear translocation. Either PKC inhibitor Go6983 or NFκB inhibitor BAY11-7082 attenuated NE-induced NOX activation, NOX2 upregulation, superoxide production, proliferation and migration.Conclusion: NE promotes oxidative stress by α-receptor/PKC/NFκB-mediated NOX2 upregulation, which contributes to proliferation and migration of VAFs.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2494314"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12024498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010118","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

Oxidative stress activates the transplanted adipose-derived stem cells to exert antioxidant effects in alopecia treatment. 氧化应激激活移植脂肪源性干细胞在脱发治疗中发挥抗氧化作用。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-06-06 DOI: 10.1080/13510002.2025.2503128

Xuer Sun, Minliang Chen

{"title":"Oxidative stress activates the transplanted adipose-derived stem cells to exert antioxidant effects in alopecia treatment.","authors":"Xuer Sun, Minliang Chen","doi":"10.1080/13510002.2025.2503128","DOIUrl":"10.1080/13510002.2025.2503128","url":null,"abstract":"Background: Alopecia is a global dermatological challenge. Adipose-derived stem cells (ADSC) show therapeutic potential, but their mechanisms in promoting hair regrowth, particularly under oxidative stress conditions, remain unclear..Objective: To investigate ADSC's role in promoting hair regrowth by mitigating oxidative stress.Methods: Using H₂O₂-stressed HaCaT cells, ADSC's protective effects were evaluated via conditioned medium (CM) and co-culture. Assessments included cell viability, colony formation, ROS, MDA, antioxidant enzymes, and 8-OHdG. Nrf2 activation was analyzed by immunofluorescence and Western blot. A mouse radiation injury model validated findings.Results: Non-pretreated ADSC offered limited oxidative protection to HaCaT cells. Conversely, H₂O₂-pretreated ADSC significantly enhanced HaCaT viability and proliferation in both CM and co-culture systems. This involved paracrine activation of the Nrf2 pathway in HaCaT cells, boosting antioxidant enzymes, accelerating ROS clearance, and reducing lipid peroxidation. These effects were reversible with Nrf2 inhibition. In vivo, CM from H₂O₂-stimulated ADSC promoted hair regrowth in irradiated mice, outperforming CM from non-pretreated ADSC by activating Nrf2 and reducing tissue oxidative damage.Conclusions: Oxidative stress potentiates the protective capacity of ADSC against oxidative via Nrf2-dependent paracrine mechanisms, offering a promising strategy for alopecia treatment.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2503128"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12147514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249411","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